1 - Review : Causes Of Chronic Pelvic Pain (CPP) In Women
Dr. Nasr Said. Nassar

2 - Chronic pelvic pain and endmetriosis
Dr. Gehan Fathy. MD

3 - Dyspareunia and Vaginismus:Review of the Literature and Treatment
Dr. Taghreid Maarouf ,MD

4 - The efficacy of (LUNA) in the treatment of unexplained chronic pelvic pain:
Hossam El-Din Shawki M.D.

5 - Case Report, A new treatment modality for women with (CPP) with unknown or undetected cause.
Dr. Nasr Said. Nassar

The Journal
Of
The Egyptian Society
Of
Chronic Pelvic Pain In Women



Chief Editor
Dr. Nasr Said Nassar______
ISSN 2090-0074 Issue No. 1 January 2009
Advisory Board
Dr. Nasr Said Nassar
Dr. Ali Mahmoud Arafa
Dr. Raoof El-Shamy
Dr. Ibtessam Said El-Arousy
Dr. Gehan Fathy
Dr. Taghreid Maarouf
Dr. Prof. Hussam El-Din Shawki

<<<<<<<<<<<<<<<<<
The Egyptian Society of Chronic Pelvic Pain in Women .
280 Terrehet El-Gabal St., El-Zaytoon, Cairo, Egypt .

Mobile Phone ( +2 ) 01014 35 991
escpp1@yahoo.com
nassarnasr@hotmail.com
www.n-w-h-f.org
( nassar women health foundation. org )
----------------------------------------
Published and Distributed for free.
Company Name: EL-SAHOWA PUBLISHING LTD
Company Number: 05810491


Contents
1– Review : Causes Of Chronic Pelvic Pain (CPP) In Women
Dr. Nasr Said. Nassar,
Consultant and Head Department of Obstetrics and Gynecology – Monira General Hospital, Cairo , Egypt. President of Egyptian Society of Chronic Pelvic Pain in Women ………………………………………………… 4
2 - Chronic pelvic pain and endmetriosis
Dr. Gehan Fathy. MD …………………………………………… 21
3 - Dyspareunia and Vaginismus:
Review of the Literature and Treatment
Dr. Taghreid Maarouf ,MD …………………………………………… 35
4 - The efficacy of Laparoscopic Uterosacral Nerve Ablation (LUNA) in the treatment of unexplained chronic pelvic pain:
A randomized controlled trial.
Hossam El-Din Shawki M.D. *Obstetrics and Gynecology Depart.
Faculty of Medicine, Menya University …………………………… 47
5 - Case Report,
A new treatment modality for women with chronic pelvic pain (CPP) with unknown or undetected cause.
Dr. Nasr Said. Nassar,
Consultant and Head Department of Obstetrics and Gynecology – Monira General Hospital, Cairo , Egypt. President of Egyptian Society of Chronic Pelvic Pain in Women ……………………………………………… 65

<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<


Review

Causes Of
Chronic Pelvic Pain (CPP) in Women

Dr. Nasr Said. Nassar,
Consultant and Head Department of Obstetrics and Gynecology – Monira
General Hospital, Cairo , Egypt.
President of Egyptian Society of Chronic Pelvic Pain in Women


Definition
Chronic pelvic pain in women refers to any pain or discomfort in the women pelvic region, the area below the belly button (umbilicus) and between both hips, that lasts six months or longer. It may or may not be associated with menstrual periods. Chronic pelvic pain is not a disease; rather, it is a symptom that can be caused by several different conditions.
Incidence
CPP is a common problem. It affects approximately 1 in 7 women (Mathias, 1996). In one study of reproductive-aged women in primary care practices, the reported prevalence rate of pelvic pain was 39% (Jamieson, 1996). Of all referrals to gynecologists, 10% are for pelvic pain (Reiter, 1990).
Causes
Various reproductive, gastrointestinal, urologic, psychological and neuromuscular disorders may cause or contribute to CPP. Sometimes, multiple contributing factors may exist in a single patient.
(Manish K Singh, MD, Assistant Professor, Pain Management, Department of Neurology, Drexel College of Medicine, Hahnemann University Hospital, Mar 2, 2006, eMedicine Specialties > Obstetrics and Gynecology > General Gynecology, http://www.emedicine.com/MED/topic2939.htmhttp://www.emedicine.com/MED/topic2939.htm)
A. Extra uterine reproductive disorders
1 Endometriosis
The presence of the endometrial tissue outside the uterine cavity leading to multiple patches of adhesions (menstrual blood not drained through the uterus)
SYMPTOMS OF ENDOMETRIOSIS
The most common symptom of endometriosis is pelvic pain. The pain often correlates to the menstrual cycle; however a woman with endometriosis may also experience pain at other times during her monthly cycle.
Pain may be felt: (varies according to the site of endometriosis)
• before/during/after menstruation
• during ovulation
• in the bowel during menstruation
• when passing urine
• during or after sexual intercourse
• in the lower back region
2 Adhesions
An adhesion is a band of scar tissue that binds 2 parts of patient`s tissue together, which should remain separate. Adhesions may appear as thin sheets of tissue similar to plastic wrap or as thick fibrous bands.
The tissue develops when the body's repair mechanisms respond to any tissue disturbance, such as surgery, infection, trauma and irradiation.
o Most adhesions are painless and do not cause complications. However, adhesions cause 60%-70% of small bowel obstructions in adults and are believed to contribute to the development of chronic pelvic pain.
o Pelvic adhesions may involve any organ within the pelvis, such as the uterus, ovaries, fallopian tubes, or bladder, and usually occur after surgery. Pelvic inflammatory disease (PID) results from an infection (usually a sexually transmitted disease) that frequently leads to adhesions within the fallopian tubes.
3 Adnexal cysts
Malignant neoplasm and benign neoplasm are uncommon in younger women but become more frequent with increasing age. In postmenopausal women with adnexal masses, both primary and secondary neoplasm must be considered, along with leiomyomas, ovarian fibromas and other lesions such as diverticular abscesses.
History, physical examination, ultrasound evaluation and selected laboratory tests will enable the physician to find the most likely cause of an adnexal mass
1 ( Diagnosis and Management of the Adnexal Mass , JANET DRAKE, M.D., University of South Florida College of Medicine, Tampa, Florida, May 15 1998 AAFP American Academy of Family Physicians )

(a) Chronic ectopic pregnancy
A ''chronic ectopic' in which repeated small bleeds have caused a haematoma (pelvic haematocele)
These patients may present with varying combinations of the following:
(1) Lower abdominal pain with or without dysurea or dysparunia .
(2) A small dark vaginal blood-loss (less than a normal period).
(3) A mass in her lower abdomen, at the side of her uterus, or in her pouch of Douglas.. Moving her cervix is painful, but this is not such a reliable sign as in an acute rupture. Her uterus is usually slightly enlarged.
(Primary Surgery: Volume One: Non-trauma Chapter 8. The surgery of pregnancy Online Edition on special wish of the editors Maurice King and Peter C. Bewes expressed on the 8th. DTC Symposium in Jena 1999 )


(b) Chlamydial endometritis or salpingitis
Sexually tranmitted urethritis, cervicitis,proctitis, endometriosis, salpingitis, and pharingitis not due to gonorrhea are caused predominantly by chlamidia and infrequently by mycoplasma or ureaplasma.
Clamydia may also cause epidedymitis, perihepattis, neonatal conjunctivitis, and infant pneumonia. Untreated Chlamydia salpingitis and endometritis can becom chronic,causing chronic pelvic pain leading to serious consequences.
Diagnosis is by culture, immunoassay for antigens, or genetic methods. Treatment is with single-dose azathromycin or a week of ofloxacin, levofloxacin, erythromycin or tetracycline.
(c) Endosalpingiosis
Endosalpingiosis is a condition in which tissue resembling that which lines the inside of the fallopian tubes is found in other areas.
Most commonly, these other areas are the outside of the fallopian tubes, ovaries or uterus. It may be found on the surface of the bowel or bladder or deeper in the uterine wall.
Endosalpingiosis is difficult to see with the naked eye. It may appear as tiny white or yellow fluid-filled cysts that make the involved surface look granular. This is a benign condition
Endosalpingiosis generally is thought to cause no symptoms. Some women may have chronic pelvic pain. but in many of these cases, endometriosis is found as well.
If endosalpingiosis is responsible for pain, it may act much like endometriosis and respond to the same treatments as endometriosis. Endometriosis frequently responds to birth control pills, Depo-Provera or Lupron. It also tends to regress during pregnancy, but pregnancy is certainly not the only means of providing relief.

(d) Ovarian retention syndrome (Residual ovary syndrome)
After hysterectomy and leaving one or both ovaries, this retained ovary (ovaries) combined with the formed local adhesions and mass causing chronic pelvic pain.
(e) Ovarian remnant syndrome
A condition where ovarian tissue is left in the pelvic cavity following the removal of ovaries and fallopian tubes causes pelvic pain. The tissue that is left behind can form cysts which can enlarge and pull on nearby adhesions causing pain.
(f) Postoperative peritoneal cysts
Peritoneal cysts are an infrequent postoperative complication.. The cysts occurred after gynecologic operations 1.5 to 8 months postoperatively. The patients presented with pain and a large pelvic mass.
(Obstetrics & Gynecology 1986;68:S53-S55)
© 1986 by The American College of Obstetricians and Gynecologists Postoperative Peritoneal Cysts, DEBRA GUSSMAN, MD, DAVID THICKMAN, MD and JAMES E. WHEEL

4 Ovulatory pain
Mittelschmerz is characterized by lower abdominal and pelvic pain that occurs roughly midway through a woman's menstrual cycle. The pain can appear suddenly and usually subsides within hours, although it may sometimes last two or three days.[1] In some women, the mittelschmerz is localized enough so that they can tell which of their two ovaries provided the egg in a given month. Because ovulation occurs on a random ovary each cycle, the pain may switch sides or stay on the same side from one cycle to another.
Diagnosis of mittelschmerz is generally made if a woman is mid-cycle and a pelvic examination shows no abnormalities. If the pain is prolonged and/or severe, other diagnostic procedures such as an abdominal ultrasound may be performed to rule out other causes of abdominal pain.
The pain of mittelschmerz is sometimes mistaken for appendicitis and is one of the differential diagnoses for appendicitis in women of child-bearing age.

5 Pelvic congestion syndrome
It is a common cause of chronic pelvic pain
 Frequency: Approximately 10% of the general female population may have pelvic varices, and 60% of those women may develop this syndrome
• Clinical Symptoms
o Chronic dull pelvic pain, pressure, and heaviness
o Often associated with movement, posture, and activities that
increase abdominal pressure
o Unilateral or bilateral
o Often asymmetric
o Physical examination findings are
varicose veins and ovarian point tenderness

• Pathophysiology
Probably multifactorial and may include:
o Dilated and tortuous ovarian veins secondary to
retrograde flow
through incompetent valves
o Obstructing anatomic anomalies as
i Retroaortic left renal vein
ii
of the left renal vein by the superior mesenteric


(Nutcracker phenomenon)
iii Right common iliac vein compression
iv Secondary congestion can be seen in various
disorders
Including:
• Valvular incompetence
• Portal hypertension
• Acquired inferior vena cava syndrome

Risk factors

Hereditary factors
Hormonal influence
Pelvic surgery
Retroverted uterus
History of varicose veins
Multiple pregnancies

Imaging Findings
o Venography
by direct visualization of dilated pelvic veins
o Transvaginal Ultrasound
By Identification of multiple dilated structures around
the uterus and ovaries with venous blood Doppler signal
The dilated pelvic vein with a diameter greater than 4mm  Slow blood flow (about 3 cm/sec)
Dilated arcuate vein in the myometrium communicating
between bilateral pelvic varicose veins
More than 50% of women have associated cystic ovaries
MR Imaging
Dilated, tortuous, enhancing tubular structures near the uterus and ovary; may see extension to the broad ligament and pelvic sidewall
T1-weighted images: varices appear as flow voids
Gradient-echo MR: varices have high signal intensity
T2-weighted images: usually varices appear low in signal intensity
3D T1 gradient-echo sequences with gadolinium: varices have high signal intensity

Treatment

Medical Treatment
May be used for underlying disorders
Procedural Treatments:
Laparoscopic transperitoneal ligation of ovarian veins
Percutaneous coil embolization of the gonadal vein
Interventional stent placement for anatomic anomalies
(SUBMITTED BY YASMIN CHAUDHRI, MD, 2005)
6 SUBACUTE SALPINGO-OOPHORITIS
Inflammation of the uterus, and fallopian tube usually caused by ascending infections of organisms from the lower reproductive tract. Salpingitis can lead to tubal scarring, hydrosalpinx, tubal occlusion, and cystic mass, Inflammation of the OVARY, generally caused by an ascending infection of organisms from the endocervix.
7 Tuberculous salpingitis
Almost always secondary to tuberculous (TB) infection elsewhere in the body. Infection may spread via the blood stream or lymphatics or, rarely, by direct extension from neighbouring organs. The main symptoms of genital TB are infertility, menstrual disorders (especially amenorrhoea) and pain.
B. Uterine reproductive disorders
1 Adenomyosis
Adenomyosis is a medical condition characterized by the presence of ectopic endometrial tissue (the inner lining of the uterus) within the myometrium (the thick, muscular layer of the uterus).
The condition is typically found in women between the ages of 35 and 50. Patients with adenomyosis can have dysmenorrhea & menorrhagia
The uterus may be imaged using ultrasound (US) or magnetic resonance imaging (MRI).
Transvaginal ultrasound is the most cost effective and most available. Either modality will show an enlarged uterus. On ultrasound, the uterus will have a heterogeneous texture, without the focal well-defined masses that characterize uterine fibroids.
2 Atypical dysmenorrhea or ovulatory pain
Mittelschmerz (German: "middle pain") is a medical term for "ovulation pain" or "midcycle pain". About 20% of women experience mittelschmerz, some every cycle, some intermittently.
SYMPTOMS AND DIAGNOSIS
Mittelschmerz is characterized by lower abdominal and pelvic pain that occurs roughly midway through a woman's menstrual cycle. The pain can appear suddenly and usually subsides within hours, although it may sometimes last two or three days.[1] In some women, the mittelschmerz is localized enough so that they can tell which of their two ovaries provided the egg in a given month. Because ovulation occurs on a random ovary each cycle, the pain may switch sides or stay on the same side from one cycle to another.
Diagnosis of mittelschmerz is generally made if a woman is mid-cycle and a pelvic examination shows no abnormalities.
The pain of mittelschmerz is sometimes mistaken for appendicitis and is one of the differential diagnoses for appendicitis in women of child-bearing age.
(FROM WIKIPEDIA, THE FREE ENCYCLOPEDIA)

3 CHRONIC ENDOMETRITIS
Endometritis refers to inflammation of the endometrium, the inner lining of the uterus. Pathologists have traditionally classified endometritis as either acute or chronic: acute endometritis is characterized by the presence of microabscesses or neutrophils within the endometrial glands, while chronic endometritis is distinguished by variable numbers of plasma cells within the endometrial stroma.
Commonly it is due to infection. Symptoms include lower abdominal pain and chronic pelvic pain, fever and abnormal vaginal bleeding or discharge.
Caesarean section, prolonged rupture of membranes and long labor with multiple vaginal examinations are important risk factors. The most common causes are chronic pelvic inflammatory disease (PID), tuberculosis, and chlamydia. Patients suffering from chronic endometritis may have an underlying cancer of the cervix or endometrium.Treatment is usually with broad-spectrum antibiotics.
4 Cervical stenosis
Cervical stenosis is stricture of the internal cervical os.
It may be congenital or acquired. The most common acquired causes are menopause, surgery (eg, conization, cautery), infection, cervical or uterine cancer, and radiation therapy.
Cervical stenosis may be complete or partial. It may result in a hematometra (accumulation of blood in the uterus) or, in premenopausal women, retrograde flow of menstrual blood into the pelvis, possibly causing endometriosis. A pyometra (accumulation of pus in the uterus) may also develop, particularly in women with cervical or uterine cancer.
Common symptoms in premenopausal women include amenorrhea, dysmenorrhea, abnormal bleeding, and infertility. Postmenopausal women may be asymptomatic for long periods. Hematometra or pyometra may cause uterine distention or sometimes a palpable mass.
Diagnosis and Treatment
Diagnosis may be suspected based on symptoms and signs or on inability to obtain endocervical cells or an endometrial sample for diagnostic tests (eg, for a Papanicolaou [Pap] test). Diagnosis of complete stenosis is established if a 1- to 2-mm diameter probe cannot be passed into the uterine cavity. If cervical stenosis causes symptoms or uterine abnormalities, cervical cytology and endometrial biopsy should be done to exclude the respective cancers.
In postmenopausal women with no history of abnormal Pap tests, no further evaluation is needed.
Treatment is indicated only if symptoms or uterine abnormalities are present and may involve cervical dilation.
5. Endometrial or cervical polyps
• Endometrial polyps
Endometrial polyps are localised overgrowths of the endometrium that project into the uterine cavity. Such polyps may be sessile (broad-based) or pedunculated (on a narrow stalk) and rarely include areas of neoplastic (benign or malignant) growth. Specifically, adenomatous hyperplasia (benign growth of the endometrium) and endometrial adenocarcinomas (malignant tumours of the glandular component of the endometrium), have been reported in only 0.6% of cases of endometrial polyps.
* The prevalence of polyps is estimated to be 10% to 24% of women undergoing hysterectomy (surgical removal of the uterus) or localised endometrial biopsy.
* Endometrial polyps are rare among women younger than 20 years of age. The incidence of these polyps rises steadily with increasing age, peaking in the fifth decade of life, and gradually declines after menopause .
• Symptoms and Signs
• Metrorrhagia is reported in 50% of symptomatic cases.
• Post-menstrual spotting is also common.
• Less frequent symptoms include hypermenorrhea , post-menopausal bleeding, and breakthrough bleeding during hormonal therapy.
Overall, endometrial polyps account for 25% of abnormal bleeding in both premenopausal and postmenopausal women.
• Endometrial polyps are often diagnosed by microscopic examination of a specimen obtained after endometrial biopsy or after D&C .
• Diagnosis and Treatment
• the diagnosis of polyps can be missed on physical exam if the uterus is not distended. Therefore, these lesions are being increasingly diagnosed by techniques such as ultrasound and hysteroscopy.
The majority of cases of endometrial polyps are cured by thorough curettage. This technique, which involves removing the endometrial lining of the uterus, is especially successful in the post-menopausal age group. However, removal of polyps or other structural abnormalities may be missed by blind curettage, therefore, hysteroscopic-guided curettage is often useful (see also D&C ). [ 1 ]
• Cervical polyps
Cervical polyps are projectile growths originating from the mucosal surface of the cervix or endocervical canal.
These small, fragile growths hang from a stalk and protrude through the cervical opening. The cause of cervical polyps is not completely understood, but they are frequently the result of infection. They may be associated with chronic inflammation, an abnormal local response to increased levels of oestrogen, or local congestion of cervical blood vessels. Cervical polyps are relatively common, especially in women over 20 years who have had children. Only a single polyp is present in most cases but sometimes 2 or 3 are found. They are rare before menarche .
Symptoms and Signs include the following:
• Abnormal vaginal bleeding: after intercourse (postcoital), after douching, between periods, after menopause.
• Menorrhagia.
• White or yellow mucous discharge (leukorrhea ).
Diagnosis and Treatment
A pelvic examination reveals smooth, red or purple, finger-like projections from the cervical canal. A cervical biopsy typically reveals mildly atypical cells and signs of infection.
Treatment involves the removal of the polyps. Removal is typically done as a simple, outpatient procedure. Gentle twisting of a cervical polyp is frequently enough to remove it, however, normally one is removed by tying a surgical ligature around the base and cutting it off. Removal of the base is done by electrocautery or laser vaporisation. Because many polyps are infected, an antibiotic may be administered after the removal, either prophylactically or with any early signs of infection. Although most cervical polyps are benign, the excised tissue should be sent to a pathologist for microscopic examination.
. Regrow of polyps is uncommon.
( Center for Uterine Fibroids: http://www.fibroids.net/ )2. Medline Plus Medical Encyclopaedia, U.S. National Library of Medicine: http://medlineplus.gov 2. Medline Plus Medical Encyclopaedia, U.S. National Library of Medicine: http://medlineplus.gov
http://www.hon.ch/Dossier/MotherChild/female_repro/external_organs.html
6 Leiomyomata
Uterine fibroids (also referred to as myoma, leiomyoma, leiomyomata, and fibromyoma) are benign (non-cancerous) tumors that grow within the muscle tissue of the uterus. Between 20-50% of women of childbearing age have uterine fibroids. While many women do not experience any problems, symptoms can be severe enough to require treatment.
Fibroids range in size from very small (coin sized) to larger than a melon. A very large uterine fibroid can cause the uterus to expand to the size of a six or seven-month pregnancy. There can either be one dominant fibroid or a cluster of many small fibroids.
Treatment options includs MR Guided focused ultrasound which destroy fibroids without incisions.
UTERINE FIBROID SYMPTOMS
Many women who have uterine fibroids have no symptoms and never require treatment. However, one out of four women of childbearing age does suffer from significant symptoms. Symptoms may vary depending on the location, size and number of fibroids.
The most common symptom of uterine fibroids is:
1. Heavy and prolonged bleeding
Anemia may result from this extensive bleeding. Abnormal bleeding is the primary uterine fibroid symptom requiring women to seek medical advice.
Other uterine fibroid symptoms may include:
• Pelvic pain or pressure
This symptom may appear as a result of the bulk or weight of the fibroids pressing on other structures in the pelvic area.
• Pain in the back of legs
This symptom appears as the fibroids press on nerves that extend to the pelvis and legs.
• Pressure on the bladder
This uterine fibroid symptom can cause frequent urination, urinary incontinence or urine retention.
• Pressure on the bowel
This can lead to constipation and/or bloating. The constipation may be exacerbated by iron supplements taken for the anemia caused by excessive bleeding.
• Lower back pain
• A feeling of pressure or fullness in the lower abdomen
• An abnormally enlarged abdomen--this may be mistaken for weight gain or pregnancy.
• Pain during sexual intercourse
Reproductive problems can also be another uterine fibroid symptom. Infertility, recurrent miscarriage, or premature labor during pregnancy can be caused by uterine fibroids.
( http://www.uterine-fibroids.org/symptoms.html )
7 Symptomatic pelvic relaxation (genital prolapse)
Uterine prolapse is descent of the uterus toward or past the introitus.
Vaginal prolapse is descent of the vagina or vaginal cuff after hysterectomy. Symptoms include vaginal pressure and fullness. Diagnosis is clinical. Treatment includes reduction, pessaries, and surgery.
A prolapsed uterus is graded based on level of descent: to the upper vagina (1st degree), to the introitus (2nd degree), or external to the introitus (3rd degree or total, sometimes referred to as procidentia). Vaginal prolapse may be 2nd or 3rd degree.
Symptoms, Signs, and Diagnosis
Symptoms tend to be minimal with 1st-degree uterine prolapse. In 2nd- or 3rd-degree uterine prolapse, fullness, pressure, and a sensation of organs falling out are common.
Third-degree uterine prolapse manifests as a bulge or protrusion of the cervix or cuff, although spontaneous reduction may occur before patients present. Vaginal mucosa may become dried, thickened, chronically inflamed, secondarily infected, and ulcerated. Ulcers may be painful or bleed and may resemble vaginal cancer. The cervix, if protruding, may also become ulcerated.
Symptoms of vaginal prolapse are similar. Cystocele or rectocele is usually present.
Diagnosis is confirmed by speculum or bimanual pelvic examination. Vaginal ulcers are biopsied to exclude cancer.
Treatment
Asymptomatic 1st- and 2nd-degree prolapse does not require treatment. Symptomatic or 3rd-degree prolapse can be treated nonsurgically if the perineum can structurally support a pessary. Severe or persistent symptoms require surgery, usually hysterectomy with surgical repair of the pelvic support structures (colporrhaphy) and suspension of the vagina (suturing of the upper vagina to a stable structure nearby). Surgery is delayed until all ulcers have healed. Vaginal prolapse is treated similarly to uterine prolapse. http://www.merck.com
8 Intrauterine contraceptive device
It is a device inserted into the uterus (womb) to prevent conception (pregnancy). The IUD can be a coil, loop, triangle, or T-shape. It can be plastic or metal.
An IUD is inserted into the uterus by a health-care professional.
C. Urologic disorders
• Chronic urinary tract infection
• Bladder neoplasm
• Interstitial cystitis
• Radiation cystitis
• Recurrent cystitis
• Recurrent urethritis
• Urolithiasis
• Uninhibited bladder contractions (detrusor-sphincter dyssynergia)
• Urethral diverticulum
• Chronic urethral syndrome
• Urethral caruncle
D. Musculoskeletal disorders
o Abdominal wall myofascial pain (trigger points)
o Compression fracture of lumbar vertebrae
o Faulty or poor posture
o Fibromyalgia
o Mechanical low back pain
o Chronic coccygeal pain
o Muscular strains and sprains
o Pelvic floor myalgia (levator ani spasm)
o Piriformis syndrome
o Rectus tendon strain
o Hernias (eg, obturator, sciatic, inguinal, femoral, spigelian, perineal and umbilical)
E. Gastrointestinal disorders
 Carcinoma of the colon
 Chronic intermittent bowel obstruction
 Colitis
 Chronic constipation
 Diverticular disease
 Inflammatory bowel disease
 Irritable bowel syndrome

F. Neurologic disorders
 Neuralgia/cutaneous nerve entrapment (surgical scar in the lower part of the abdomen; usually iliohypogastric, ilioinguinal, genitofemoral, and lateral femoral cutaneous nerves)
 Shingles (herpes zoster infection)
 Degenerative joint disease
 Disk herniation
 Spondylosis
 Abdominal epilepsy
 Abdominal migraine
 Neoplasia of spinal cord or sacral nerve
G. Psychologic and other disorders
 Personality disorders
 Depression
 Sleep disorders
 Sexual and/or physical abuse

We will discuss later , in detailes about each of the previous causes , in this journal.







Chronic pelvic pain and endmetriosis
Dr. Gehan Fathy. MD
-------------------------------
Chronic pelvic pain is common in women in the reproductive age group and it causes disability and distress and results in significant costs to health services. The pathogenesis of chronic pelvic pain is poorly understood.
Chronic pelvic pain (CPP) refers to pain of at least six months' duration that occurs below the umbilicus and is severe enough to cause functional disability or require treatment. In fact, CPP is considered the principal indication for approximately 20 percent of all hysterectomies performed for benign disease and at least 40 percent of all gynecological laparoscopies performed annually in the United States [1,2].
The five major sources that should be considered in evaluating women with CPP are:
• Gastrointestinal
• Urological
• Gynecological
• Psychological
• Musculoskeletal
• Neurological
Endometriosis has been reported in 25 to 38 percent of adolescents with chronic pelvic pain [2, 3]. The prevalence among adolescents undergoing laparoscopy for pelvic pain not controlled with oral contraceptive pills (OCPs) and nonsteroidal anti-inflammatory drugs (NSAIDs) is 50 to 70 percent [4-6].
PATHOGENESIS — Some adolescents may have a genetic predisposition to developing endometriosis. Although a tendency to develop endometriosis may be inherited, the pathogenesis of endometrial tissue outside the uterus is still debated. Many theories have been proposed to explain the etiology of endometriosis, and no one theory accounts for all presentations. The implantation or retrograde menstruation theory proposes that endometrial tissue from the uterus is shed during menstruation and transported through the fallopian tubes, thereby gaining access to and implanting on pelvic structures [10] ,The coelomic metaplasia theory proposes that the coelomic cavity contains undifferentiated cells capable of dedifferentiating into endometrial tissue [14],the cellular immunity theory, which is the most recently proposed hypothesis, suggests that a deficiency in cellular immunity allows ectopic endometrial tissue to proliferate [16-18]. No single theory explains all cases of endometriosis, especially when relating to adolescents and postpubertal/premenarchal endometri.
The ectopic implants develop a sensory and sympathetic nerve supply similar to that of the healthy uterus [46]. In the rat model, this supply connects the implants directly with the central nervous system via the splanchnic and vagus nerves [12, 13]. Input to the spinal cord from the implants arrives at the same spinal segments as those receiving input from the ureter but rostral to segments receiving input from the vaginal canal or bladder. Thus, vaginal hyperalgesia and ureteral pain in this rat model likely involve central neural mechanisms [12, 13], whereas the effects of endometriosis on bladder function could be via peripheral interactions and/or in the caudal spinal cord.
Two other factors may help to explain the variable types and severity of endometriosisassociated pains,First, their co-occurrence with other painful disorders, and their amelioration by a hypoestrogemc state: (i) central sensitization, and (ii) divergent and convergent connectivity in the central nervous system. By means of several molecular processes [14], sensitization of the sensory fibers would in turn produce central sensitization, which is a long-lasting hyperexcitability of neurons in the central nervous system that can continue long after the originally sensitized input is reduced or eliminated (e.g., by surgery).Second, sensory input arriving at the spinal cord from individual internal organs diverges within the cord. Thus, although information from different organs is delivered most densely to spinal neurons within the entry segments, it is also delivered, less densely, to widespread spinal regions extending for many segments rostrally and caudally [12]. These results suggest that inconsistency in the various pains associated with the ectopic implants could reflect variability in a number of factors associated with the implants' nerve supply. These factors include the types of nerves that innervate the implants, agents that activate or sensitize them, sites in the central nervous system where the nerves deliver information, and how that information is modulated by estradiol-both peripherally [15] and centrally [16].
Much remains to be learned about how endometriosis comes to be associated so variably with pain symptoms and how those symptoms are ameliorated by a hypoestrogenic state. One promising area of research concerns the implants' sensory and autonomic nerve supply and its potentially estradiol-modulated influence on activity within the central nervous system.
Pelvic pain assessment form — The International Pelvic Pain Society has developed a detailed approach to facilitate obtaining the history and performing the physical examination in women with CPP .This document includes :
Pain history — A complete history of the patient's pain, as well as a thorough review of systems with emphasis on symptoms of urinary tract disease, bowel disease, reproductive tract disease, musculoskeletal disorders, and psychoneurological disorders is essential. Any history of prior treatments; substance dependence; sexual, physical, or psychological abuse; and domestic violence should also be sought.
The characteristics of the pain should be noted, including first occurrence, location, intensity, quality, duration, temporal pattern, precipitating and alleviating factors, relationship to urination and defecation, and patterns of radiation. A monthly pain calendar in which the patient records episodes of pain, location, severity, and associated factors (eg, menses, mood, use of medication, bowel/bladder function, coitus and other physical activities) can also be useful for obtaining this information and response to treatment. It is also important to develop an understanding of the effect of CPP on the woman's life: work, school, social activities, relationships, exercise, sleep, and other areas of concern to the patient.
This information can help in differential diagnosis:
• Pain that is dull and diffuse and whose location is difficult for the patient to determine is often visceral. In contrast, the patient usually can accurately describe the specific location of somatic pain.
• Cyclic pelvic pain, especially if associated with severe dysmenorrhea, is often due to a hormonally responsive condition, such as endometriosis or adenomyosis. Onset of pain during pregnancy or immediately postpartum suggests a musculoskeletal etiology, sometimes referred to as "peripartum pelvic pain syndrome" [7].
• Pain that first develops prior to menarche is unlikely to have a gynecologic etiology.
• Dysmenorrhea is almost always the initial pain symptom in a patient with endometriosis associated pelvic pain.
• Referred pain is aching and perceived to be near the surface of the body.
• Pain associated with nerve entrapment is characteristically described as hot or burning, or as electric shock-like pain. Paresthesia is common with nerve entrapment, as well.
• Pain that is aggravated by the urge or need to void usually suggests interstitial cystitis, and is much less commonly associated with endometriosis or irritable bowel syndrome.
• Symptoms that occur in relation to abdominal pain may give important information. Weight loss may occur in association with malignancy, nausea and vomiting with bowel obstruction, and change in bowel habits with a colonic lesion.
Pain map — Asking the patient to complete a pain map can be helpful for localizing pain. Pain maps may show that the patient also has pain outside of the pelvis, such as headaches or low back pain, or may reveal a dermatomal distribution or along a myotome, suggesting a nonvisceral source.
PSYCHOLOGICAL ASSESSMENT — A tool for assessing psychological status is provided in the International Pelvic Pain Society's patient evaluation form.
Some simple screening questions for depression and physical/sexual abuse include [13] :
• During the past month, have you felt down, depressed or hopeless?
• During the past month, have you felt little interest or pleasure in doing things?
• Have you ever been touched against your will?
Further laboratory testing is based on the clinical impression that emerges after a complete history and physical examination, as well as laboratory and imaging studies.
Imaging — Pelvic ultrasound is highly sensitive for identifying pelvic masses and determining the origin of the mass (ovary, uterus, fallopian tube). It is less reliable for distinguishing between benign and malignant neoplasms and diagnosing adenomyosis. Sonography is particularly useful for detecting small pelvic masses (less than 4 cm in diameter), which often cannot be palpated on bimanual examination. Magnetic resonance imaging is obtained in some cases to better define an abnormality suspected by sonography [17] and for diagnosis of adenomyosis.
Laparoscopic surgery — The role of laparoscopy in the evaluation of women with CPP is uncertain. The absence of visible pathology does not exclude a physical basis for the patient's pain, but does exclude several common disorders which can be visualized at surgery (endometriosis, adnexal mass, adhesions, some uterine abnormalities, PID) [20] . Nevertheless, the use of laparoscopy in women with CPP should be individualized since histologic diagnosis of endometriosis is not mandatory before medical therapy, adhesiolysis is not necessarily effective for relief of CPP, and adnexal masses and uterine abnormalities can be diagnosed noninvasively by ultrasound.
Laparoscopic pain mapping — Conscious laparoscopic pain mapping refers to laparoscopy performed under local anesthesia in which the tissues are probed and pulled with surgical instruments while the patient is asked about the severity and nature of any pain she perceives. An etiology may be suggested if the pain induced by iatrogenic manipulation replicates the patient's chronic pain. Ideally, this information would allow a targeted approach to subsequent medical and surgical therapy. The role of conscious laparoscopic pain mapping is unclear, as there are no data from controlled studies showing improvement in outcomes [21,22] .


TREATMENT OF PELVIC PAIN — Women with pelvic pain and suspected endometriosis may be managed with empiric medical therapy prior to establishing a definitive diagnosis by laparoscopy [4, 5]. It is suggested to start with analgesics and/or combined oral contraceptives for women with no more than mild pelvic pain and a GnRH agonist for those with moderate to severe pelvic pain. Although 80 to 90 percent of patients will have some improvement in symptoms with medical therapy, medical interventions neither enhance fertility nor diminish endometriomas or adhesions [6-8]. Therefore, women with suspected endometriomas and advanced stages of disease, or infertility, are more appropriately managed surgically.
Medical treatment of mild pain
Analgesics — Although NSAIDs are commonly used for analgesia, there are no high quality data showing that they are effective for managing pain due to endometriosis or more effective than other agents [9] . Use of NSAIDs is based on their ready availability, low cost, acceptable side effect profile.
Oral contraceptive pills — Oral contraceptive pills (OCPs) are a good choice for women with minimal or mild symptoms who also want to prevent pregnancy. An advantage of OCPs over most other hormonal interventions is that they can be taken indefinitely.
OCPs induce decidualization and subsequent atrophy of endometrial tissue, including ectopic endometrial tissue. For most patients with only mild pain, use of OCPs relieves dysmenorrhea [10-12] It is unclear whether a cyclic, continuous, or tricycle regimen is most effective [6]. If pain does not respond well to cyclic therapy, switching to continuous OCP administration may be effective [10].
Medical treatment of moderate or severe pain — hormonal interventions other than OCPs to women with early stage disease who are not achieving adequate pain relief after a three- to six-month trial with analgesics or OCPs and to those with recurrent mild endometriosis and pain. The rationale for use of hormonal intervention is that altering the patient's estrogen/progesterone profile should affect the course of the disease since ovarian steroids affect the growth of endometriosis.
The three hormonal interventions (other than OCPs) most commonly used to treat endometriosis are gonadotropin-releasing hormone (GnRH) agonist analogs, danazol, and progestins. GnRH analogs and danazol induce a state of "pseudomenopause," whereas progestins alone or in combination with estrogen hormonally mimic pregnancy.
GnRH agonists — we suggest use of a GnRH agonist for treatment of moderate to severe pain associated with endometriosis. Randomized trials have shown that GnRH agonists are as effective as other medical therapies for relieving pain and reducing the size of endometriotic implants [19]. With add-back therapy, side effects are often better tolerated than those associated with a progestin or danazol. Similar to other medical treatments, GnRH agonists do not enhance fertility [8].
GnRH agonists can be administered by daily nasal spray, or intramuscular injections every one to three months. Generally, initial treatment with a GnRH agonist is continued for six months. An empiric trial of GnRH agonist therapy, without surgical/histological confirmation of disease, is reasonable in patients with dysmenorrhea or chronic pelvic pain who have not responded to NSAIDs or OCPs, and in whom other causes of chronic pelvic pain have been excluded by history, physical examination, and laboratory testing [20]. Baseline tests, such as a complete blood count with differential and erythrocyte sedimentation rate, urinalysis, and testing for chlamydia and gonorrhea infection, are obtained to screen for a chronic infectious or inflammatory process. Pelvic ultrasound is highly sensitive for identifying pelvic masses and determining the origin of the mass (ovary, uterus, fallopian tube).
A detailed discussion of the use and efficacy of GnRH agonists for treatment of endometriosis can be found separately.
Progestins — Progestins inhibit endometriotic tissue growth by causing decidualization initially, and then atrophy. They also inhibit pituitary gonadotropin secretion and ovarian hormone production. In randomized trials and prospective observational studies, progestins alone, at appropriate doses, were an effective treatment of pelvic pain caused by endometriosis: over 80 percent of women had partial or complete pain relief with this therapy [21-23]. The effectiveness of progestins in eliminating implants and the risk of recurrent endometriosis following treatment is less well-documented. A few studies have reported significantly reduced implant scores (determined at laparoscopy) after progestin therapy [21,24] .A few small studies, including one randomized trial, reported that the levonorgestrel-releasing intrauterine contraceptive device (Lng-IUC) reduced both chronic pelvic pain and dysmenorrhea in women with endometriosis [25,26] . Irregular menstrual bleeding and amenorrhea are common side effects.
Progesterone antagonists — Progesterone antagonists and selective progesterone receptor modulators have also been used successfully in pilot studies of treatment of endometriosis [27]. Use of these agents led to a reduction of both nonmenstrual pelvic pain and dysmenorrhea. Possible mechanisms include inhibition of endometrial proliferation, a direct suppressive effect on endometrial blood vessels, and suppression of endometrial prostaglandin production.
Danazol — Danazol is effective in resolving implants when treating mild or moderate stages of disease and over 80 percent of patients experience relief or improvement of pain symptoms within two months of treatment [28,29] . danazol cause dose-dependent side effects, and a small percentage of patients discontinue the drug because of them. Side effects include weight gain, muscle cramps, decreased breast size, acne, hirsutism, oily skin, decreased high density lipoprotein levels, increased liver enzymes, hot flashes, mood changes, and depression.
Aromatase inhibitors — Although not approved for the treatment of pelvic pain caused by endometriosis, use of aromatase inhibitors is a novel approach. These agents appear to regulate local estrogen formation within the endometriotic lesions themselves, in addition to inhibiting estrogen production in the ovary, brain, and adipose tissue [30] .In multiple case reports and small series, aromatase inhibitors have been used (off-label) successfully to interrupt this pathway in the treatment of severe endometriosis [31-33] .It is important to remember that aromatase inhibitors cause significant bone loss with prolonged use and cannot be used as single agents in premenopausal women.
Surgical management — Indications for surgical management of endometriosis include:
• Symptoms that are severe, incapacitating, or acute (as with rupture or torsion of an endometrioma)
• Symptoms that have failed to resolve or have worsened under medical management
• Presence of advanced disease (eg, anatomic distortion of the pelvic organs, endometriotic cysts, or obstruction of the bowel or urinary tract)
• Patient reluctance to use hormonal/non-surgical treatments
Conservative surgery — Conservative surgery preserves the uterus and as much ovarian tissue as possible. A laparoscopic approach offers advantages over laparotomy, including a shorter duration of hospitalization, anesthesia, and recuperation [34] . Laparotomy may be necessary when dealing with extensive adhesions or invasive endometriosis located near structures such as the uterine arteries, ureter, bladder, and bowel. Ancillary procedures to laparotomy may include presacral neurectomy, uterosacral interruption of sensory nerves innervating the pelvis, and uterine suspension to avoid adhesion formation from the cul-de-sac to the posterior surface of the uterus, tube, and ovaries.
Pain relief is achieved in most patients who undergo laparoscopic ablation of endometriosis and adhesiolysis [35] . However, the risk of recurrence is estimated to be as high as 40 percent at 10 years of follow-up [36]. laparoscopic laser ablation of endometriotic implants plus uterine nerve ablation was more likely to result in improvement or resolution of symptoms at six months than expectant management (63 versus 23 percent) [37] . Women with stage I disease were less likely to improve after their surgical procedure than women with stage II-IV disease.
The degree of pain relief achieved with conservative surgery may be enhanced by presacral neurectomy [38,39] .
Definitive surgery — Definitive surgery involves hysterectomy, with or without removal of the fallopian tubes and ovaries. Definitive rather than conservative surgery for treatment of endometriosis should be considered when (1) incapacitating symptoms persist following conservative surgery, (2) moderate to severe disease is present and future pregnancy is not desired, or (3) hysterectomy is indicated for coexisting pelvic pathology. The decision to perform a definitive procedure is primarily dependent upon the patient's interest in maintaining child-bearing potential. Young women (under the age of 30 years) who undergo hysterectomy are more likely than older women to report residual symptoms, a sense of loss, and overall disruption in their life [38].
The ovaries may be conserved in younger women to avoid premature development of menopausal symptoms and decisions regarding estrogen replacement.
Combination medical/surgical therapy
Preoperative medical therapy — Hormonal suppression has been used prior to surgery to decrease the size of endometriotic implants, thereby reducing the extent of surgery required [39]. However, there is no evidence that preoperative hormonal intervention decreases the extent of surgical dissection required to remove implants, prolongs the duration of pain relief, increases future pregnancy rates, or decreases recurrence rates.
Postoperative medical therapy — Progestins, danazol, or GnRH agonists have been used in conjunction with laparotomy or laparoscopic conservative or definitive surgical treatment. Several trials have reported postoperative therapy using one of these agents increased the duration of pain relief and delayed recurrence of disease [40,41].
Although uncommon, some experts suggest postsurgical hormonal intervention to treat "microscopic" implants and thus delay recurrence. A pilot study examining this issue randomly assigned 40 parous women with moderate to severe endometriosis undergoing first-line laparoscopic excision/ablation of endometriotic lesions to immediate insertion of a Lng-IUC or expectant management [26]. Moderate or severe dysmenorrhea recurred in 2 of 20 women in the Lng-IUC group versus 9 of 20 women managed expectantly one year after surgery.
TREATMENT OF SYMPTOMS RELATED TO DEEP ENDOMETRIOSIS — Deep endometriosis is a term used to describe infiltrative forms of the disease that involve the uterosacral ligaments, rectovaginal septum, bowel, ureters or bladder. The origin is probably intraperitoneal endometriotic implants that have invaded and caused inflammation of the involved tissue. Another potential etiology is growth of retroperitoneal müllerian remnants.
Asymptomatic disease is managed expectantly [42]. Medical therapy of symptomatic disease is generally ineffective or transiently effective, with recurrence rates approaching 70 percent [43]. Surgical therapy is effective for relieving pelvic pain, dyspareunia, and painful defecation [44]. Surgical resection does not enhance future pregnancy rates [45].There is no consensus on the extent of resection necessary to treat deep endometriosis. Extensive dissection in the rectovaginal septum and rectal wall dissection are often necessary and require the skill of an experienced surgeon. Performing hysterectomy and bilateral salpingoophorectomy alone is inadequate definitive therapy if endometriosis involving the bowel is left untreated. In these cases, bowel resection may be necessary [46].
Treatment of pain
• For women with no more than mild pelvic pain, nonsteroidal antiinflammatory drugs could be suggested over other medical interventions . For women who also desire contraception, oral contraceptive pills is suggested .
• For women with moderate pain who are not achieving adequate pain relief with nonsteroidal antiinflammatory drugs and/or combined oral contraceptive pills, and those with recurrent mild endometriosis and pain, a GnRH agonist is preferable over other hormonal therapies
• For women who want to avoid the high cost and risk of bone loss associated with GnRH agonists, progestins have a more favorable side effect profile than danazol.
• For women with symptoms that are severe, incapacitating, or acute (rupture or torsion of an endometrioma), or who have advanced disease (eg, anatomic distortion of the pelvic organs, endometriotic cysts, or obstruction of the bowel or urinary tract), surgical rather than medical therapy is the management of choice . For women in whom surgery did not result in complete removal of implants, postoperative medical therapy is suggested to increase the duration of pain relief and delay recurrence of symptoms.
Treatment of deep endometriosis
• For women with pelvic pain, dyspareunia, or painful defecation related to deep endometriosis, we suggest surgical rather than medical therapy
There is no high quality evidence that one medical therapy is superior to another for managing pelvic pain due to endometriosis. Therefore, treatment decisions are individualized, taking into account the severity of symptoms, the extent and location of disease, whether there is a desire for pregnancy, the age of the patient, medication side effects, surgical complication rates, and cost.
Treatment options include:
• Expectant management
• Analgesia
• Hormonal medical therapy
- Combined oral contraceptive pills, cyclic or continuous
- Gonadotropin-releasing hormone (GnRH) agonists
- Progestins, given by an oral, parenteral, or intrauterine route
- Danazol
- Aromatase inhibitors
• Surgical intervention, which may be conservative (retain uterus and ovarian tissue) or definitive (removal of the uterus and possibly the ovaries)
• Combination therapy in which medical therapy is given before and/or after surgery
Laparoscopy is the gold standard for establishing the diagnosis of endometriosis, and provides an opportunity for conservative surgical treatment. Therapeutic intervention is desirable at this time to ablate or excise implants and adhesions, thus potentially preventing or delaying disease or symptom progression. Early surgical therapy also avoids the expense and side effects of medical therapy. Potential disadvantages include inadvertent damage to adjacent organs (especially the bowel and bladder), postoperative infectious complications, and mechanical trauma to pelvic structures that may result in greater adhesion formation.

1. Vessey, MP, Villard-Mackintosh, L, Painter, R. Epidemiology of endometriosis in women attending family planning clinics. BMJ 1993; 306:182.
2. Moen, MH. Is a long period without childbirth a risk factor for developing endometriosis?. Hum Reprod 1991; 6:1404.
3. Parazzini, F, La Vecchia,C, Franceschi, S, et al. Risk factors for endometrioid, mucinous and serous benign ovarian cysts. Int J Epidemiol 1989; 18:108.
4. ACOG Committee Opinion. No. 310. Obstet Gynecol 2005; 105:921.
5. ACOG practice bulletin. Medical management of endometriosis. No. 11. Clinical management guidelines for obstetrician-gynecologists. Int J Gynaecol Obstet 2000; 71:183.
6. Kennedy, S, Bergqvist, A, Chapron, C, et al. ESHRE guideline for the diagnosis and treatment of endometriosis. Hum Reprod 2005; 20:2698.
7. Hughes, E, Brown, J, Collins, JJ, et al. Ovulation suppression for endometriosis. Cochrane Database Syst Rev 2007; :CD000155.
8. Allen, C, Hopewell, S, Prentice, A. Non-steroidal anti-inflammatory drugs for pain in women with endometriosis. Cochrane Database Syst Rev 2005; :CD004753.
9. Vercellini, P, Frontino, G, De Giorgi, O, et al. Continuous use of an oral contraceptive for endometriosis-associated recurrent dysmenorrhea that does not respond to a cyclic pill regimen. Fertil Steril 2003; 80:560.
10. Vercellini, P, Trespidi, L, Colombo, A, et al. A gonadotropin-releasing hormone agonist versus a low-dose oral contraceptive for pelvic pain associated with endometriosis. Fertil Steril 1993; 60:75.
11. Proctor, ML, Roberts, H, Farquhar, CM. Combined oral contraceptive pill (OCP) as treatment for primary dysmenorrhoea (Cochrane Review). Cochrane Database Syst Rev 2001; 4:CD002120.
12. Buttram, VC Jr. Cyclic use of combination oral contraceptives and the severity of endometriosis. Fertil Steril 1979; 31:347.
13. Strathy, JH, Molgaard, CA, Coulam, CB, Melton LJ, 3rd. Endometriosis and infertility: a laparoscopic study of endometriosis among fertile and infertile women. Fertil Steril 1982; 38:667.
14. Kirshon, B, Poindexter AN, 3rd. Contraception: a risk factor for endometriosis. Obstet Gynecol 1988; 71:829.
15. Parazzini, F, La Vecchia, C, Franceschi, S, et al. Risk factors for endometrioid, mucinous and serous benign ovarian cysts. Int J Epidemiol 1989; 18:108.
16. Moen, MH. Endometriosis in women at interval sterilization. Acta Obstet Gynecol Scand 1987; 66:451.
17. Moen, MH. Is a long period without childbirth a risk factor for developing endometriosis?. Hum Reprod 1991; 6:1404.
18. Davis, L, Kennedy, SS, Moore, J, Prentice, A. Modern combined oral contraceptives for pain associated with endometriosis. Cochrane Database Syst Rev 2007; :CD001019.
19. Prentice, A, Deary, AJ, Goldbeck-Wood, S, et al. Gonadotrophin-releasing hormone analogues for pain associated with endometriosis. Cochrane Database Syst Rev 2000; :CD000346.
20. 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; 93:51.
21. Telimaa, S, Puolakka, J, Ronnberg, L, Kauppila, A. Placebo-controlled comparison of danazol and high-dose medroxyprogesterone acetate in the treatment of endometriosis. Gynecol Endocrinol 1987; 1:13.
22. Prentice, A, Deary, AJ, Bland, E. Progestagens and anti-progestagens for pain associated with endometriosis. Cochrane Database Syst Rev 2000; :CD002122.
23. Crosignani, PG, Luciano, A, Ray, A, Bergqvist, A. Subcutaneous depot medroxyprogesterone acetate versus leuprolide acetate in the treatment of endometriosis-associated pain. Hum Reprod 2006; 21:248.
24. Dawood, MY, Obasiolu, CW, Ramos, J, et al. Clinical, endocrine, and metabolic effects of two doses of gestrinone in treatment of pelvic endometriosis. Am J Obstet Gynecol 1997; 176:387.
25. Vercellini, P, Aimi, G, Panazza, S, et al. A levonorgestrel-releasing intrauterine system for the treatment of dysmenorrhea associated with endometriosis: a pilot study. Fertil Steril 1999; 72:505.
26. Vercellini, P, Frontino, G, De Giorgi, O, et al. Comparison of a levonorgestrel-releasing intrauterine device versus expectant management after conservative surgery for symptomatic endometriosis: a pilot study. Fertil Steril 2003; 80:305.
27. Chwalisz, K, Perez, MC, Demanno, D, et al. Selective progesterone receptor modulator development and use in the treatment of leiomyomata and endometriosis. Endocr Rev 2005; 26:423.
28. Barbieri, RL, Evans, S, Kistner, RW. Danazol in the treatment of endometriosis: Analysis of 100 cases with a 4-year follow-up. Fertil Steril 1982; 37:737.
29. Selak, V, Farquhar, C, Prentice, A, Singla, A. Danazol for pelvic pain associated with endometriosis. Cochrane Database Syst Rev 2007; :CD000068.
30. Attar, E, Bulun, SE. Aromatase inhibitors: the next generation of therapeutics for endometriosis?. Fertil Steril 2006; 85:1307.
31. Shippen, ER, West, WJ Jr. Successful treatment of severe endometriosis in two premenopausal women with an aromatase inhibitor. Fertil Steril 2004; 81:1395.
32. Amsterdam, LL, Gentry, W, Jobanputra, S, et al. Anastrazole and oral contraceptives: a novel treatment for endometriosis. Fertil Steril 2005; 84:300.
33. Hefler, LA, Grimm, C, van Trotsenburg, M, Nagele, F. Role of the vaginally administered aromatase inhibitor anastrozole in women with rectovaginal endometriosis: a pilot study. Fertil Steril 2005; 84:1033.
34. Crosignani, PG, Vercellini, P, Biffignandi, F, et al. Laparoscopy versus laparotomy in conservative surgical treatment for severe endometriosis. Fertil Steril 1996; 66:706.
35. Jacobson, TZ, Barlow, DH, Garry, R, Koninckx, P. Laparoscopic surgery for pelvic pain associated with endometriosis. Cochrane Database Syst Rev 2001; :CD001300.
36. Wheeler, JM, Malinak, LR. Recurrent endometriosis: Incidence, management, and prognosis. Am J Obstet Gynecol 1983; 146:247.
37. Sutton, CJ, Ewen, SP, Whitelaw, N, Haines, P. Prospective, randomized, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis [see comments]. Fertil Steril 1994; 62:696.
38. MacDonald, SR, Klock, SC, Milad, MP. Long-term outcome of nonconservative surgery (hysterectomy) for endometriosis-associated pain in women<30 years old. Am J Obstet Gynecol 1999; 180:1360.
39. Yap, C, Furness, S, Farquhar, C. Pre and post operative medical therapy for endometriosis surgery. Cochrane Database Syst Rev 2004; :CD003678.
40. Hornstein, MD, Hemmings, R, Yuzpe, AA, Heinrichs, WL. Use of nafarelin versus placebo after reductive laparoscopic surgery for endometriosis. Fertil Steril 1997; 68:860.
41. Abou-Setta, AM, Al-Inany, HG, Farquhar, CM. Levonorgestrel-releasing intrauterine device (LNG-IUD) for symptomatic endometriosis following surgery. Cochrane Database Syst Rev 2006; :CD005072.
42. Fedele, L, Bianchi, S, Zanconato, G, et al. Is rectovaginal endometriosis a progressive disease?. Am J Obstet Gynecol 2004; 191:1539.
43. Shaw, RW. Treatment of endometriosis. Lancet 1992; 340:1267.
44. Donnez, J, Nisolle, M, Gillerot, S, et al. Rectovaginal septum adenomyotic nodules: a series of 500 cases. Br J Obstet Gynaecol 1997; 104:1014.
45. Vercellini, P, Pietropaolo, G, De Giorgi, O, et al. Reproductive performance in infertile women with rectovaginal endometriosis: is surgery worthwhile?. Am J Obstet Gynecol 2006; 195:1303.
46. Darai, E, Ackerman, G, Bazot, M, et al. Laparoscopic segmental colorectal resection for endometriosis: limits and complications. Surg Endosc 2007; 21:1572.



Dyspareunia and Vaginismus:
Review of the Literature and Treatment
Dr. Taghreid Maarouf ,MD

Sexual pain disorders—dyspareunia and vaginismus—are controversial entities [1]. An intense debate is ongoing on the “real” nature of dyspareunia (is it a “sexual” or a “pain” disorder?) and on its partial overlap with vaginismus [2]. Recent research has demonstrated persistent problems with the sensitivity and specificity of the differential diagnosis of these two phenomena [3]. However, as no consensus has been reached in unifying the two entities, they will be kept separate according to the latest classifications [4].
The etiology of sexual pain disorders is multifactorial, with different attention paid to biological [1,4] versus psychodynamic factors [3], according to the prominent background of the researchers, particularly in the case of dyspareunia.
Dyspareunia and vaginismus are sensitive issues, as this type of pain involves emotionally charged behaviors: sexual intimacy and vaginal intercourse [3]. Pain encompasses a complex perceptive experience, involving psychological and relational meanings, which may become increasingly important with the chronicity of pain [1]. Unfortunately, most patients have been denied for years that their pain was real: “Pain is all in your head” was a common theme of diagnostic neglect.
Definition
The last published consensus defines dyspareunia as “persistent or recurrent pain with attempted or complete vaginal entry or penile-vaginal intercourse” [5].
Vaginismus indicates persistent or recurrent difficulties of the woman to allow vaginal entry of a penis, a finger, or any object, despite the woman’s expressed wish to do so.
There is often (phobic) avoidance and anticipation, fear, or experience of pain, along with variable involuntary pelvic muscle contraction. Structural or other physical abnormalities must be ruled out and addressed [5].
Prevalence
Dyspareunia is reported by 12% to 15% of premenopausal, coitally active women [6]. After menopause, dyspareunia is often comorbid with vaginal dryness, causing introital friction and pain of variable intensity. Around 26% to 37% of women not on hormone replacement therapy complain of dyspareunia [7]. Vaginismus may occur in 0.5% to 1% of fertile women, although precise estimates are lacking [7].
Etiology and Pathophysiology of Dyspareunia
Dyspareunia is the common symptom of a variety of coital pain-causing etiologies summarized. Factors predisposing to dyspareunia with documented odds ratios are reviewed by Latthe et al. [6]. Curiously, this last published meta-analysis [6] does not mention vulvar vestibulitis (VV), vulvodynia, or other frequent etiologies of dyspareunia, indicating the biases that are still present in research. Different etiologies may cause similar pathophysiologic processes when they trigger an inflammatory response. According to the site where pain
is perceived and the estrogenic “age” (pre- or postmenopause), the biologic etiologies more frequently recognized in the clinical practice are briefly reviewed here to facilitate the clinician in his/her pathophysiologically based diagnostic approach.
Premenopausal women
Causes of introital dyspareunia
1-VV is a subset of vulvodynia [3,8]. The diagnostic triad is the following: 1) severe pain upon vestibular touch or attempted vaginal entry; 2) exquisite tenderness to cottonswab palpation of the introital area (mostly at 5 and 7 o’clock, when looking at the introitus as a clock face); and 3) dyspareunia [9]. From the pathophysiologic point of view, VV involves the upregulation of three systems. First is the immunologic system, introital mast-cells, with hyperproduction of both inflammatory molecules and nerve growth factors (NGF), which may be upregulated by recurrent Candida infections, mechanical trauma, or chemical or physical damages[7,10]. Second is the pain system, with proliferation of local pain fibers induced by the NGF, which may contribute to the hyperalgesia and allodynia, associated with neuropathic pain reported by patients with VV [7,10]. Third is hyperactivity of the levator ani, which can be antecedent to VV and comorbid with mild vaginismus [8,12] or secondary to the introital pain [12]. In either case, addressing the muscular component is a key part of treatment [1,7]. Hyperactivity of the pelvic floor causes a reduction of the introital opening, literally squeezed by the contracted surrounding muscle. It is a predisposing factor, contributing to introital dyspareunia (when the erected penis “forces” the narrower introitus), increasing the vulnerability of the vaginal mucosa to the microabrasions caused by the mechanical trauma of thrusting in unlubricated conditions (pain is the strongest reflex inhibitor of vaginal lubrication) [1,7].
It can also contribute to urethralgia and trigonal pain associated with sex, with a spectrum of lesion potentially progressing from postcoital cystitis to interstitial cystitis, two of the most frequent urologic comorbidities of dyspareunia [1,11]. Lack of vaginal lubrication is associated with impaired or absent congestion of periurethral vessels, thus exposing the urethra to the coital mechanical trauma[7,12].
2- Hyperactivity of the pelvic floor may be triggered by nongenital, nonsexual causes, such as urologic conditions like recurrent cystitis and interstitial cystitis or coloproctologic diseases (irritable bowel syndrome, ulcerative colitis) and anorectal problems (anismus, hemorrhoids, rhagades) [11].
3- Postpartum genital pain is the leading etiology of introital dyspareunia in lactating women. Vaginal dryness, secondary to the hypoestrogenic state when the woman is breastfeeding, may be worsened by poor episiorrhaphy outcome [12].
4- A fibrous, cribrous, septate, or circinate hymen prevents penetration. Patients may spend years in psychotherapy for dyspareunia when the etiology of coital pain is simply removed by hymenectomy or hymenal incision with local anesthesia.[7]
Causes of deep dyspareunia
1-Endometriosis is one of the leading etiologies of chronic pelvic pain in fertile women This disease should be considered when the woman reports invalidating dysmenorrhea, painful ovulation, pelvic pain, and pain at deep vaginal examination or when the disease has been histologically diagnosed after laparoscopy. [12,13].
2- Pelvic inflammatory disease (PID) is the leading cause of deep dyspareunia, chronic pelvic pain, and infertility. It is secondary to infective damage or obstruction of the salpinges bilaterally, usually caused by Chlamydia trachomatis [6].
Postmenopausal women
Causes of introital dyspareunia
1-Vaginal dryness, secondary to loss of estrogens, is the most frequent contributor to introital dyspareunia after menopause [12,14].
2- Lichen sclerosus is an autoimmune disease associated with thinning and whitening of the vulvar skin, narrowing of the vaginal introitus, and involution of the vascular and cavernosal tissues, contributing to genital arousal disorder and dyspareunia [12,14].
3-Sjِgren’s syndrome is an autoimmune disease in which antibodies are produced against exocrine glands, including Bartholin’s gland, and contributes to vaginal dryness and introital dyspareunia[7,14].
Etiology and Pathophysiology of Vaginismus
Two major etiologies include fear of penetration, up to a frank phobia of intercourse, and primary neurodystonia of the pelvic floor, as recently demonstrated with needle electromyography [14]. The generalized anxiety associated with fear of penetration is somatized in a general muscular arousal, which may cause a defensive contraction of the perivaginal muscles, leading to vaginismus [12,15]. These etiologies may overlap. Vaginismus may be so severe as to prevent penetration
completely [16], thus becoming the leading cause of unconsummated marriages in women. When of moderate intensity, it allows for painful penetration, causing lifelong dyspareunia [8,12]. Comorbidity between lifelong vaginismus and dyspareunia and other female sexual disorders is frequently reported [8,17]
Clinical Approach
Talking with patients about sexual pain disorders requires special attention to the sensitivity of the issue and an empathic attitude to the biological “truth” of pain [7,12]. Location and characteristics of pain have been demonstrated to be the most significant predictors of the etiology of pain [12,18]. No instrumental exam so far is more informative than a comprehensive clinical history and a carefully performed clinical examination.
History taking
Key questions to obtain the most relevant information can be summarized as follows:
-Did you experience coital pain from the very beginning of your sexual life onwards (lifelong) or did you experience it after a period of normal
(painless) sexual intercourse (acquired disorder)?
-If lifelong, were you afraid of feeling pain before your first intercourse?
-If acquired, do you remember the situation or what happened when it started?
-Where does it hurt? At the opening of the vagina, in the mid-vagina, or deep in the vagina? Location of the pain and its onset within an episode of intercourse are the strongest predictors of presence and type of organicity.
-When do you feel pain: before, during, or after intercourse?
-Do you feel other accompanying symptoms, such as vaginal dryness, pain, or paresthesias in the genitals and pelvic areas?
- Do you suffer from cystitis 24 to 72 hours after intercourse?
-How intense is the pain you feel?
-Do you remember any negative event (neglect, poor sexual education, harassment, abuse) that, in your opinion, could be associated with your current pain at intercourse?
-How is your relationship? Are you happy with it or do you recognize emotional/affective factors or conflicts that may predispose or worsen your pain?
-Do you think that the size of your partner’s penis may contribute to your pain?
Physical examination
A mandatory component of diagnosis is a competent physical examination, general and genital, to describe the “pain map” (ie, any site in the vulva, introitus, mid-vagina, and deep vagina where pain can be elicited.
The physician should note the following:
--Pelvic floor trophism (and vaginal pH); muscular tonus, strength, and performance; and myogenic and referred pain
--Signs of inflammation (primarily VV)
--Poor outcome of pelvic or perineal surgery (episiotomy/episiorrhaphy)
Associated signs of urogenital and rectal pain syndromes
--Neuropathic pain in vulvodynia or localized clitoralgia with no objective findings

In patients with vaginismus, the diagnosis and prognosis may be determined based on three variables: 1) intensity of the phobic attitude (mild, moderate, severe)
toward penetration ; 2) intensity of the pelvic floor hypertonicity (in four degrees, according to Lamont ; and 3) coexisting personal or relational psychosexual problems .
Exams
In selected cases, the clinician may require the following:

●Hormonal profile, when dyspareunia is associated with vaginal dryness or when other symptoms suggest impending menopause, premature or not
●Pelvic ultrasonography, in patients with deep dyspareunia, when the history suggests pelvic endometriosis or PID or diagnostic laparoscopy
●Levator ani electromyography in cases of severe vaginismus, for research purposes
●Vaginoscopy in the case of suspected transversal vaginal septum

Principles of Treatment of Sexual Pain Disorders
Sexual comorbidity is a key issue in sexual pain disorders. Dyspareunia and vaginismus, because of coital pain, directly inhibit genital arousal and vaginal receptivity. Indirectly, they may affect (coital) orgasmic potential during intercourse and impair physical and emotional satisfaction, causing loss of desire for and avoidance of sexual intimacy [1,8,14].
Dyspareunia is best cured when the pathophysiology of coital pain is understood and addressed. Consensuson the best treatment protocol has not yet been reached,
given the heterogeneity of etiologies of dyspareunia and the controversy on the etiology and “real” features of vaginismus. In the author’s experience, a pathophysiologically based therapy is the most effective. Deep dyspareunia, secondary to endometriosis, PID, chronic pelvic pain, and other less frequent etiologies, requires a specialist treatment that goes beyond the scope
of this paper.

Medical treatment
Multimodal therapy
VV should be treated with a combined, multimodal treatment aimed at reducing the following:
1-The upregulation of mast cells, by reducing the agonist stimuli (such as Candida infections) with oral treatment with fluconazole or itraconazole, eliminating microabrasions of the introital mucosa with temporal coital abstinence, and reducing
chemicals or allergens by improving lifestyles that cause degranulation leading to chronic tissue inflammation or with antagonist modulation of its hyperreactivity with amitriptyline [12,13].
2-The upregulation of the pain system secondary to both the proliferation of introital pain fibers [19] induced by NGF produced by the upregulated mastcells,
and the lowered central pain threshold [20]. Analgesic treatment should be prescribed locally, with electroanalgesia or, in severe cases, with ganglion impar block [20] or systemically, with a tricyclic antidepressant. Gabapentin
or pregabalin, two inhibitors of neuronal firing, are indicated in the most severe cases, with a neuropathic component [7,12].
3-The upregulation of the muscular response, with hyperactivity of the pelvic floor, which may precede VV when the predisposing factor is vaginismus [1,7] or acquired in response to genital pain [1,12]. In controlled studies,
electromyographic feedback has been demonstrated to significantly reduce pain in patients with VV. Self-massage, pelvic floor stretching, and physical therapy may reduce the muscular component of coital pain [21]. When hyperactivity of
the pelvic floor is elevated, treatment with type A botulinum toxin has been proposed on the basis of its efficacy and safety profile [12].

Practical tip
Patients and couples should abstain from vaginal intercourse and use other forms of sexual intimacy during VV treatment, until introital pain and burning feelings have
disappeared, to prevent the persistence of introital microabrasion
caused by penetration.

Topical hormones
Vaginal estrogen treatment is the first choice (when no contraindications are present) when dyspareunia is associated with genital arousal disorders and hypoestrogenism contributing to vaginal dryness, in long-lasting hypothalamic
amenorrhea, puerperium, and postmenopause. The safety of hormonal topical treatment is confirmed by different studies . Vulvar treatment with testosterone (1% or 2% testosterone in oil or petroleum jelly) may be considered when vulvar dystrophy or lichen sclerosus contributes to introital dyspareunia.[22]

Psychosexual treatment
Psychosexual and behavioral therapy
A combined approach—psychosexual, pharmacologic, and rehabilitative—is the most effective. Selective serotonin reuptake inhibitors are indicated to modulate the intense systemic arousal in the subset of severely phobic patients [7,12]. Anxiety,
depression, fear of pain, and sexual avoidant behaviors should be addressed. The shift from pain to pleasure is key from the sexual point of view. Sensitive and committed psychosexual support of the woman and the couple is mandatory.
Vaginismus
Vaginismus should be treated with a multimodal approach, given its complex neurobiologic, muscular, and psychosexual etiology [23]. Best outcomes are
obtained by integrating several types of therapy.

Pharmacologic therapy
Selective serotonin reuptake inhibitors and anxiolytics are indicated to modulate the severe phobic attitude [7]. Type A botulinum toxin, injected in the levator ani, when the patient is able to accept the injection, is indicated in severe myogenic hyperactivity. Its use is still investigational [7]. In couples who do not desire pregnancy, hormonal contraception should be discussed before the first intercourse together with other alternative methods.

Psychosexual and behavioral therapy
Underlying negative affects (fear, disgust, repulsion to touch), loss of self-esteem and self-confidence, and body image concerns [23] should be addressed. Sexual education is essential in case of restrictive upbringing. If the woman has a current partner, active, nonpenetrative sex play should be encouraged to maintain or increase libido, arousal, and possibly clitoral orgasm [23]. Once the phobic attitude is reduced and voluntary pelvic floor relaxation obtained, permission should be given for more intimate play, and insertion of the penis with the woman in control. Psychotherapy, sex therapy, or couples therapy is recommended when significant psychodynamic or relationship issues are evident.

Rehabilitative therapy
Rehabilitation of the pelvic floor is the core of the physical change. The physical therapist teaches the patient how to recognize muscle tension and how to command and relax the pelvic floor muscles [21,23]. When the patient accepts the vaginal probe, electromyographic feedback may enhance and accelerate the learning on muscle control. When good voluntary pelvic floor relaxation has been obtained, dilators of different size are inserted under pelvic floor relaxation [12,23].

Practical tip
The couple should be supported during first attempts, both emotionally and pharmacologically (when indicated, with phosphodiesterase type 5 inhibitors for the partner). The concepts of “symptom inducer” and “symptom carrier” should turn attention to couple dynamics in every phase of the treatment.

Conclusions
Dyspareunia has a multifactorial etiology. The associated hyperactive pelvic floor contributes to medical and psychosexual comorbidities. Vaginismus may cause lifelong dyspareunia when mild to moderate and may prevent intercourse when severe. Sexual pain disorders require a multidisciplinary approach. Physicians have a prominent role in the diagnosis and treatment of sexual pain disorders in their biological etiology and associated medical comorbidities. Psychotherapists and sexologists address the psychodynamic and relational contributors. Physical
therapists are essential in relaxing the pelvic floor to reduce both sexual pain and pelvic floor–related medical comorbidities. The uroandrologist is also part of the team when the male partner presents with a concomitant sexual disorder that should be diagnosed and addressed.

Referrence
1.• Graziottin A: Treatment of sexual dysfunction. In Evidence Based Physiotherapy For The Pelvic Floor—Bridging Research and Clinical Practice. Edited by Bo K, Berghmans B, van Kampen M, Morkved S. Oxford: Elsevier; 2007:277–287.
2. Meana M, Binik YM, Khalife S, Cohen D: Dyspareunia: sexual dysfunction or pain syndrome? J Nerv Ment Dis 1997, 185:561–569
3. Pukall C, Lahaie M, Binik Y: Sexual pain disorders: etiologic factors. In Women’s Sexual Function and Dysfunction: Study, Diagnosis, and Treatment. Edited by
Goldstein I, Meston CM, Davis S, Traish A. London: Taylor and Francis; 2005:236–244.
4. Abramov L, Wolman I, David M: Vaginismus: an important factor in the evaluation and management of vulvar vestibulitis syndrome. Gynecol Obstet Invest 1994, 38:194–197.
5. Basson R, Leiblum S, Brotto L, et al.: Revised definitions of women’s sexual dysfunction. J Sex Med 2004, 1:40–48.
6. Latthe P, Mignini L, Gray R, et al.: Factors predisposing women to chronic pelvic pain: systematic review. BMJ 2006, 332:749–755.
7. Graziottin A: Sexual pain disorders: dyspareunia and vaginismus. In Standard Practice in Sexual Medicine. Edited by Porst H, Buvat J. Oxford: Blackwell; 2006:342–350.
8. Engman M, Wijma K, Wijma B: Itch and burning pain in women with partial vaginismus with or without vulvar vestibulitis. J Sex Marital Ther 2007, 33:171–186.
9. Oskai U, Baj N, Yalcin O: A study on urogenital complaints of postmenopausal women aged 50 and over. Acta Obstet Gynecol Scand 2005, 84:72–78
10. Bachmann G, Rosen R, Pinn V, et al.: Vulvodynia: a state-of-the-art consensus on definitions, diagnosis and management J Reprod Med 2006, 51:447–456.
11. Peters KM, Killinger KA, Carrico DJ, et al.: Sexual function and sexual distress in women with interstitial cystitis: a case control study. Urology 2007, 70:543–547.
12. Graziottin A, Rovei V: Sexual pain disorders. In Sexual Health. Edited by Owens AF, Tepper MS. Westport, CT: Praeger; 2007:287–313.
13. Ferrero S, Esposito F, Abbamonte L: Quality of sex life in women with endometriosis and deep dyspareunia. Fertil Steril 2005, 83:573–579
14. Graziottin A: Sexuality in postmenopause and senium. In Current Management of Menopause. Edited by Lauritzen C and Studd J. London: Martin Duniz; 2004:185–203.
15. Payne KA, Binik YM, Amsel R, Khalife S: When sex hurts, anxiety and fear orient attention towards pain. Eur J Pain 2005, 9:427–436
16. Leiblum S: Vaginismus: a most perplexing problem. In Principles and Practice of Sex Therapy, edn 3. Edited by Leiblum SR, Rosen RC. New York: Guilford Press;
2000:181–204.
17. Graziottin A: Sexual pain disorders in adolescents. In Proceedings of the 12th World Congress of Human Reproduction , International Academy of Human Reproduction. Rome: CIC Edizioni Internazionali; 2005:434–449
18. Graziottin A, Brotto LA: Vulvar vestibulitis syndrome: a clinical approach. J Sex Marital Ther 2004, 30:125–139
19. Bornstein J, Goldschmid N, Sabo E: Hyperinnervation and mast cell activation may be used as histopathologic diagnostic criteria for vulvar vestibulitis. Gynecol Obstet Invest 2004, 58:171–178.
20. Pukall CF, Binik YM, Khalife S, et al.: Vestibular tactile and pain thresholds in women with vulvar vestibulitis syndrome. Pain 2002, 96:163–175.
21. Rosenbaum TY: Physiotherapy treatment in sexual pain disorders J Sex Marital Ther 2005, 31:329–340.
22. North American Menopause Society: The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of the North American Menopause Society. Menopause 2007, 14:355–369.
23. Crowley T, Richardson D, Goldmeier D; BASHH Special Interest Group for Sexual Dysfunction: Recommendations for the management of vaginismus: BASHH Special Interest Group for Sexual Dysfunction. Int J STD AIDS 2006,17:14–18.


The efficacy of Laparoscopic Uterosacral Nerve Ablation (LUNA) in the treatment of unexplained chronic pelvic pain:
A randomized controlled trial.
Hossam El-Din Shawki M.D.
*Obstetrics and Gynecology Depart. Faculty of Medicine, Menya University
Objective: The 1ry aim of this work is to explore the efficacy and the safety of LUNA in relief of pain in women with chronic pelvic pain in whom diagnostic laparoscopy reveals either no pathology or mild endometriosis (AFS score ≤ 5). The 2ry aim was evaluate the patients' satisfaction from the procedure during 3, 6 and 12 months follow up and to test the hypothesis that response to LUNA differs according to type of the pain by two secondary analyses: (I) Women with primary or secondary dysmenorrhea, (II) women with deep dysparonia.
Study Design: A prospective single blind randomized trial with 12 months follow up.
Setting: Obstetrics and Gynecology Depart. Faculty of Medicine, Menya University, Menya, Egypt.
Patients: Forty eight patients was chronic pelvic pain, with free diagnostic laparoscopy eligible to randomization into tow equal groups, 1st group, control group, laparoscopy without pelvic denervation and the 2nd group, study group, laparoscopy with Uterosacral nerve ablation.
Intervention: Diagnostic laparoscopy with or without laparoscopic Uterosacral nerve ablation.
Results: The efficacy was comparable between group I and group II at three, six and twelve months of follow up (P≤0.05). Also, the overall success rate between group I and group II was comparable to each other as it was 75%, 75% and 66.66% versus 79.16%, 79.16% and 75% at three, six and twelve months respectively(P≤0.05). Patients' Satisfaction rate did not varied significantly between group I and group II at 3, 6, 12 months follow up, ( P≤0.05). The cumulative satisfaction rate was 75%, 75% and 70.83% versus 79.16%, 79.16% and 70.83% at 3, 6, 12 months between group I and group II respectively (P≤0.05). There was a statistically significant difference between both groups as regarding the effectiveness of laparoscopic Uterosacral nerve ablation (LUNA) in treatment of primary (spasmodic) dysmenorrhea and deep dysparonia, (P≥0.05), on the other hand as regarding the effectiveness of LUNA in treatment of secondary (congestive) dysmenorrhea there was no statistically significant difference between both groups (P≤0.05). As regarding safety, there were no statistically significant difference between group I and group II concerning the occurrence of intraoperative complications (P≤ 0.05), while on the other hand ,the postoperative complications, as constipation, urinary urgency and uterine prolapsed were more frequently to occur among patients of the 2nd group(P≥ 0.05).
¬¬¬In conclusion: Accumulating data from the present study, shown that LUNA can be an option in a well selected circumstances, specially for control of menstrual pain without endometriosis; however, its effectiveness may not extend to other indications, such as secondary dysmenorrhea associated with endometriosis but it considered as an option in patients without a cause in diagnostic laparoscopy. Also, preliminary experience in the treatment of primary deep dyspareunia, presenting a promising perspective yet without sufficient evidence on the management of deep dyspareunia. A randomized controlled study with an adequate number of patients is warranted.
Key Words: chronic pelvic pain, LUNA, dysmenorrhea, laparoscopy.
E-mail: Hossam20002003@yahoo.com


Introduction:
Chronic pelvic pain (CPP) can be defined as intermittent or constant pain in the lower abdomen or pelvis of at least 6 months’ duration, not occurring exclusively with menstruation or intercourse and not associated with pregnancy; it is a symptom, not a diagnosis (1). Dysmenorrhea, deep dyspareunia, and intermenstrual pain constitute its main symptom complex (2).
Chronic pelvic pain (CPP) is one of the commonest symptomatology in gynecological outpatient clinics. It accounts for 10% of office visits to gynecologists [3] , general clinics [4], and According to Renaer [5], CPP accounts for about a quarter of out- patient consultations in general gynecological practice and for 40–60% of all diagnostic laparoscopies. Chronic pelvic pain (CPP) has a profound impact on a woman’s personal health and quality of life, including an economic impact through loss of working hours (2).
The objective evaluation of (CPP) poses a complex task as most of the times physical signs are absent, most of the times patients are treated symptomatically or referred to psychiatrist as somatoform disorder without adequate diagnostic evaluation [6], so laparoscopy is a valuable tool in the evaluation of undiagnosed CPP. Laparoscopy can establish a definite diagnosis and modify the treatment without resorting to exploratory laparotomy. It is also an extremely valuable adjunct in gynecologist's armamentarium especially in confirming minimal disease and adhesions, which cannot be revealed sonographically (7). In the mean time, the cause of the pain is not always obvious as no pathology is seen in 40–60% of the cases(8). In the absence of pathology there is no established treatment , therefore treatment of chronic pelvic pain is sometimes unsuccessful, and hysterectomy often becomes the final resort(9). Therefore, a conservative surgery, if shown to be effective, would represent a major improvement in its management(2).
The presence of nerve plexuses and ganglia in the Uterosacral ligaments has been known for over a century(10). The Lee-Frankenhauser sensory nerve plexuses and parasympathetic ganglia in the Uterosacral ligaments carry pain from the uterus, cervix and other pelvic structures(8), and ablation of these nerve plexuses and ganglions has been performed for many years through abdominal or vaginal routes. However, recent developments in minimal access surgery using laparoscopy (using laser or electrocautery), make Uterosacral nerve ablation a practicable treatment option ,which is called laparoscopic Uterosacral nerve ablation (LUNA) (2&8).
There are widespread variations in the LUNA technique without reliable evidence of effectiveness(11). Fortunately, some recent reports of randomized controlled studies have clarified some roles of LUNA in the control of pelvic pain(12-13). However, the balance of benefits and risks of this intervention have not been reliably assessed. LUNA has, nevertheless, been introduced into practice, although there remains controversy regarding indications for LUNA. Hence, there is an urgent need for a randomized controlled trial to confirm, or refute, any worthwhile effectiveness, and to assess the principal of hypothesis that, in women with chronic pelvic pain in whom diagnostic laparoscopy reveals either no pathology or mild endometriosis (AFS score ≤ 5) ,LUNA alleviates pain and improves life quality (8).
Systematic review [14] has shown that the currently available research evidence on LUNA is inconclusive. Therefore further research is required to generate effectiveness evidence in the form of a high quality randomized controlled trial. This need is also supported by the recent Cochrane Reviews [15,16] that recommend vigorous research to assess surgical interventions in chronic pelvic pain.
Aim of the Work:
The 1ry aim of this work is to explore the efficacy and the safety of LUNA in relief of pain in women with chronic pelvic pain in whom diagnostic laparoscopy reveals either no pathology or mild endometriosis (AFS score ≤ 5). The 2ry aim was evaluate the patients' satisfaction from the procedure during 3,6 and 12 months follow up and to test the hypothesis that response to LUNA differs according to type of the pain by two secondary analyses: (I) Women with primary or secondary dysmenorrhea, (II) women with deep dysparonia.
Patients and Methods:
This prospective randomized-controlled-trial is conducted at the endoscopy unite of the Gynecology department , El-Menya University hospital between the period of Jun 2004 to Jun 2007 with single blind assessment of outcomes in eligible consenting patients randomized at diagnostic laparoscopy to LUNA (study group) or to no pelvic denervation (control group). The primary assessment of the effectiveness of LUNA will be from comparison of outcomes at the one-year follow-up.
Eligibility:
All new patients (86 women ) presenting to the Gynecology outpatient clinic with pelvic pain (cyclical or noncyclical) and/or dyspareunia, and requiring diagnostic laparoscopy for evaluation of these conditions, will be invited to participate . When they consent to participate, they are registered prior to randomization .Only 48 patients was eligible to randomization into one of both of the study groups according to the following criteria(8):
1-Inclusion criteria
• Pelvic pain of longer than 6-month duration.
• Pain located within the true pelvis or between and below the anterior iliac crests.
• Associated functional disability.
• Lack of response to medical treatment.
• Planned diagnostic laparoscopy with no pelvic pathology.
2-Exclusion criteria
• Previous LUNA.
• Mild, moderate and severe endometriosis (American Fertility Society score >5).
• Previous surgery for endometriosis.
• Previous surgery for pelvic inflammatory disease.
• Previous hysterectomy.
• Adnexal pathology.
Selected patients were thoroughly counseled and informed consent was taken from all the patients. Complete history was taken including the patients present symptoms, past medical history, medication used, known allergies, and previous similar attack (s) and method(s) of treatment. A detailed general, abdominal, and pelvic examination were preformed, including a vaginal examination using sterile speculum. Cervical cytology, pelvic and vaginal ultrasound was done for all patients. Also, complete hematological and biochemical investigations were . At this point, the women were randomly assigned to diagnostic laparoscopy to start therapy according to the following protocol that has been approved by the medical ethical committee of the department.
Interventions:
Routine preparation will be made for a diagnostic laparoscopy with the patient under general anesthesia. Following pneumoperitoneum, a laparoscope will be used to visualize the pelvis. Before embarking on operative laparoscopy an anatomical pelvic assessment will be performed to identify pelvic structures and pathology. At this stage patients with pathology outlined in the exclusion criteria will be excluded. It is expected that around 30% to 50% of women will be unsuitable for LUNA at operation and will be 'registered only' cases. Eligible patients will be randomized into one of the study groups 1st group, control group, laparoscopy without pelvic denervation and the 2nd group, study group, laparoscopy with Uterosacral nerve ablation [17].
The posterior leaf of the broad ligament will be carefully inspected to identify the course of the ureters, which on rare occasions could be particularly close to the Uterosacral ligaments. Care will also be taken to note thin walled pelvic veins, which often lie lateral to the Uterosacral ligaments. If accidentally punctured, they may cause troublesome bleeding requiring further endoscopic endocoagulation. The Uterosacral ligaments will be identified by manipulation of the uterus in the right and left lateral planes. Clear identification of the Uterosacral ligaments is a prerequisite for treatment and ablation of the ligament will carried out using 5mm bipolar electro-diathermy using bipolar Myerland forceps(the main unite of the diathermy is adjusted at 30 W, and energy is applied to 5 seconds in order to deliver a dose power of coagulation 150 J to every Uterosacral ligament) before complete transaction of the Uterosacral ligaments ,using a 5 mm curved siccoser that supplied with the ability to use monopolar electro-diathermy if needed, is done. The ablation will start as close to the posterior aspect of the cervix as possible and continue for a minimum of 1 cm posterolaterally on either side. The aim of the procedure is to destroy the sensory nerve fibers and the secondary ganglia as they leave the uterus and come to lie within the Uterosacral ligaments(8).
The safe conduct of operative laparoscopy for LUNA requires the use of two ports, one for delivery of the energy source ( diathermy) and another for manipulation. These are in addition to the umbilical port used for the laparoscope itself.
Following surgery, the surgeon, fills the operation details on a post-surgery form, including the laparoscopic finding, technique, the operative time, intra operative blood loss, intra operative and postoperative complications . Also, after the operation, at discharge, the patients were asked to record their degree of pain by means of a visual analog scale( 1=no pain, 2=minimal pain, 3=tolerable pain, 4=sever pain and 5= not tolerable pain). The discharge time , and the interval to return to the normal activity were recorded for all patients.
Randomization
Consenting patients (86 patients) will subjected to diagnostic laparoscopy first, then Consenting eligible patients (48 patients) will be randomized into two equal groups including 24 patients in the control group (diagnostic laparoscopy with no pelvic denervation ) and 24 patients in the study group( diagnostic laparoscopy plus Uterosacral nerve ablation).The patients will be allocated to groups using a chance procedure, blocking and stratification [18]. Stratified block randomization will be employed to ensure that there will be nearly equal numbers of patients in the two groups within the prognostic subgroups, even if the study ends prematurely so that chance imbalances in the stratification variable do not have an effect on the outcome.
Blinding
In this study, patients will be kept blind to their treatment allocation until the follow-up in the trial is complete to avoid the placebo effect ( that may occurred) if they know they have received the active treatment [19]. Unfourntally, single blind approach was used as it was difficult to keep the surgeon blind to the procedure.
Follow up protocol: -
All patients were followed up after 3,6, and 12 months after the ablation. Follow up visits included : history taking, clinical examination, ultrasound (abdominal and vaginal ) examination, and cytological evaluation. The success rate was defined as the percentage of women who reported no, minimal or tolerable pain during the period of follow up and without hystererectomy or repeated LUNA. The patients’ satisfication was estimated by by asking the patient direct question( did the procedure improve your health status ?), and the patients’ answer will determine the degree of satisfaction {it is excellent (4) , good (3), average (2) or no improvement (1)}. Also all patients were followed up for long term complication, and the need for additional treatment (medical or surgical ) which was considered as treatment failure.
Statistical analysis:
Statistical analysis was preformed on an IBM personal computer using SPSS statistical package for windows ( SOSS,Inc,USA). Results were expressed as mean ±SD for quantitative characteristics and number and percentage for qualitative characteristics. Among different groups statistical comparison were made using Chi-square X2 test or Fisher exact test for qualitative characteristics for qualitative characteristics and One way analysis of variance ANOVA for numerical results among different groups. P values of ≤ 0.05 were cosidered as the level of significance.


Results:
There were no statistically significant differerance between both groups regarding demographic and clinical characteristics of patients( table I). The efficacy (that was evaluated by the percentage of women who reported no, minimal or tolerable or sever pain during the period of follow up and without hysterectomy or repeated LUNA.) was comparable between group I and group II at three , six and twelve months of follow up . These results after 3 months were ,41.61%, 20.83%, 12.60% and 25% versus 45.83%, 25%, 8.33% and 20.83% between group I and group II respectively and at six months were 37.50%, 20.83%, 16.66% and 25% versus 30% ,29.16% ,8.33% and 20.83% between group I and group II respectively while at twelve months were 33.33%, 16.66%, 16.66% and 33.33% versus 37.50%, 25%, 12.16% and 29.16% between group I and group II respectively (P≤0.05). Also the overall success rate between group I and group II was comparable to each other as it was 75%, 75% and 66.66% versus 79.16%, 79.16% and 75% at three, six and twelve months respectively(P≤0.05)(Table III). Patients' satisfaction rate did not varied significantly between group I and group II at 3, 6, 12 months follow up, as it was excellent in 54.16 %, 50 %, and 45.83 % versus 58.33 %, 58.33% and 50% at 3, 6 and 12 months between group I and group II respectively, it was good in 8.33%, 12.60%, and8.33% versus 12.60%, 8.33% and 8.33% at 3, 6 and 12 months between group I and group II respectively, it was moderate in 12.60%,12.60%,and 12.60% versus 8.33%, 12.60% and 12.60% at 3, 6 and 12 months between group I and group II respectively, and no improvement in 25%, 25%,and 33.33% versus 20.83%, 20.83% and 29.16% at 3, 6 and 12 months between group I and group II respectively.( P≤0.05). The cumulative satisfaction rate was 75% , 75% and 70.83% versus 79.16%, 79.16% and 70.83% at 3, 6, 12 months between group I and group II respectively (P≤0.05) (Table VI). The effectiveness of laparoscopic Uterosacral nerve ablation (LUNA) (when compared to a control or no treatment) in treatment of primary (spasmodic) dysmenorrhea, there was a statistically significant difference between both groups , as The cumulative success rate was 42.85% , 42.85% and 28.57% versus 83.33%, 100% and 100% at 3, 6, 12 months between group I and group II respectively (P≥0.05) , also as regarding pain relief score among patients with dysparonia, there was a statistically significant difference between both groups as the cumulative success rate was 66.66% , 55.55% and 44.44% versus 80%, 90% and 90% at 3, 6, 12 months between group I and group II respectively (P≥0.05) , on the other hand as regarding the effectiveness of LUNA in treatment of secondary ( congestive ) dysmenorrhea there was no statistically significant difference between both groups , as The cumulative success rate was 75% , 62.50% and 62.50% versus 71.42%, 71.42% and 71.42% at 3, 6, 12 months between group I and group II respectively (P≤0.05) (Table V). There were no statistically significant difference between group I and group II concerning the occurrence of bleeding, uterine perforation ,visceral injuries, vascular injuries or conversion to open surgery (P≤ 0.05), while on the other hand there were statistically significant difference between group I and group II as regarding the postoperative complications, as constipation, urinary urgency and uterine prolapsed were more frequently to occur among patients of the 2nd group(P≤ 0.05)(Table III).

Table I :Clinical Characteristics of patients in both treatment groups:
Group I ( Control)
No= 24 Group II ( study)
No= 24 P value
1-Age ( years) range: ( mean ± SD) 25-45
31.90±2.44 24-43
30.25 ± 2.55 N.S
2-Weight (kg) range: ( Mean ± SD) 48-75
66-11±5.31 50-72
67.18 ± 4.34 N.S
3- Height (cm) range: ( Mean ± SD) 153-170
163±1.17 152-173
161 ± 2.10 N.S
4-BMI ( kg/ m2) range: ( Mean ± SD) 24.40 – 29.55
24.80 ± 1.46 23.66 – 28.41
25.23 ± 1.25 N.S
5-Parity ( No) range: ( Mean ± SD) 1-8
4.78 ±1.65 1-7
5.43 ± 1.61 N.S
*6-Clinical presentation(s): (N-%)
Acyclic lower abdominal pain
Congestive dysmenorrhea.
Spasmodic dysmenorrhea.
Deep dysparonia.

10(41.66%)
8(33.33%)
7(29.16%)
9 (37.50%)

11(45.83%)
7(29.16%)
6(25.00%)
10(41.66%)

N.S
N.S
N.S
N.S

**7-Pervaginal findings : (N-%)
A-Pelvic tenderness :
Localized to one fornix
Bilateral
Diffuse
B-Fornical fullness :
Unilateral
Bilateral
C-Culde-sac nodularity
D-Fixed retroverted uterus
E-No significant finding
15 (62.50%)
4 (16.66%)
3 (12.60%)
8 (33.33%)
10 (41.61%)
4 (16.66%)
6 (25%)
3 (12.60%)
1 (4.16%)
9 (37.50%)
16(66.66%)
5 (20.83%)
3 (12.60%)
8 (33.33%)
9 (37.50%)
5 (20.83%)
4 (16.66%)
2 (8.33%)
1 (4.16%)
8 (33.33%)
N.S
N.S
N.S
N.S
N.S
N.S
N.S
N.S
N.S
N.S
*Eight patients (33.33%) in each group had more than one presentation
**Ten patients (41.61%) in each group had more than one pervaginal findings

Table II : Operative and postoperative data for both treatment groups
Group I
No= 24 Group II
N= 24 P value
Operative time Rang ( Min) ;
( Mean ± SD) 25- 35
27.50 ± 4.51 30-48
36.33 ±7.68 S
Intraoperative complications : ( N- %)
Bleeding
Uterine Perforation
Visceral injuries.
Vascular injuries.
Conversion to open surgery.

1(4.16%)
1(4.16%)
0
0
0
2(8.33%)
1(4.16%)
0
0
0
N.S
N.S
N.S
N.S
N.S
Discharge time Range ' days' :
( mean ± SD) 1-2
1.33 ± 0.22 1-2
1.33 ± 0.22 N.S
*Post operative complications : (N-%)
Fever
Postoperative bleeding
Constipation
Urinary urgency
Uterine prolapse.
Painless labor
4(16.66%)
0
0
0
0
0
5(20.83%)
0
3(12.60%)
4(16.66%)
2(8.33%)
0
N.S
N.S
S
S
S
N.S
Time to return to normal life style ) range: ' days'(mean± SD) 4-10
6.78 ± 1.55 5-10
6.34 ±1.22
N.S
*Including immediate and remote complications during the period of follow up
Table III : Pain score after treatment at 3, 6, 12 month follow up in both groups:
Group I(N=24) Group II (N=24) P value
3MS 6MS 12MS 3MS 6MS 12MS
(1)No pain N-% 10(41.61%) 9(37.50%) 8(33.33%) 11(45.83%) 10 (30%) 9(37.50%) N.S.
(2) Minimal pain N-% 5(20.83%) 5 (20.83%) 4 (16.66%) 6 (25.00%) 7(29.16%) 6 (25.00%) N.S.
(3)Tolerable pain N-% 3(12.60%) 4 (16.66%) 4 (16.66%) 2( 8.33%) 2 (8.33%) 3 (12.60%) N.S.
(4)Sever Pain N-% 6 (25.00%) 6 (25.00%) 8 (33.33%) 5 (20.83%) 5 (20.83%) 7 (29.16%) N.S.
Over all succ. Rate (18/24) (75%) (18/24) (75%) ( 16/ 24) 66.66% (19/ 24) 79.16% (19/ 24) 79.16 % (18/ 24)
75% N.S.


Table IV : Satisfaction rate of the treatment group 3, 6, 12 months follow up in both groups:
Group I Group II P value
3MS 6MS 12MS 3MS 6MS 12MS
Excellent 13
(54.16%) 12
(50.00%) 11
(45.83%) 14
(58.33%) 14
(58.335%) 12
(50.00%) N.S
Good 2
( 8.33%) 3
(12.60%) 2
( 8.33%) 3
(12.60%) 2
( 8.33%) 2
( 8.33%) N.S.
Moderate 3
(12.60%) 3
(12.60%) 3
(12.60%) 2
( 8.33%) 3
(12.60%) 3
(12.60%) N.S
No improvement 6 (25.00%) 6 (25.00%) 8
(33.33%) 5 (20.83%) 5 (20.83%) 7 (29.16%) N.S.
*Cumulative satisfaction rate 18 (75.00%) 18 (75.00%) 17
(70.83%) 19 (79.16%) 19
(79.16%)
17 (70.83%) N.S
Cumulative satisfaction rate= Excellent+Good+ Moderate.

Table V : Pain score after treatment in relation to different types of chronic pelvic pain at 3, 6, 12 month follow up in both groups
Group I Group II P value
Acyclic lower abdominal pain N=10 Acyclic lower abdominal pain N=11
3MS 6MS 12MS 3MS 6MS 12MS
No pain N-% 3(30%) 2(20%) 2(20%) 5(45.45%) 5(45.45%) 6(54.54%) S
Minimal pain
N -% 2(20%) 1(10%) 1(10%) 3(30%) 218.18%) 1(9.09%) N.S.
(3)Tolerable pain N-% 1(10%) 2(20%) 1(10%) 2(18.18%) 2(18.18%) 1(9.09%) N.S.
(4)Sever Pain N-% 4(40%) 5(50%) 6(60%) 1(9.09%) 2(18.18%) 3(27.27%) S
5- cumulative success rate 6(50%) 5(50%) 6(60%) 10(90.90%) 9(81.81%) 8(72.72%)
Congestive dysmenorrhea N=8 Congestive dysmenorrheal N=7
(1)No pain N-% 1(12.5%) 1(12.5%) 2(25%) 1(14.28%) 2(28.57%) 2(28.57%) NS
(2) Minimal pain N-% 3(37.5%) 2(25%) 2(25%) 2(28.57%) 2(28.57%) 2(28.57%) NS
(3)Tolerable pain N-% 2(25%) 2(25%) 1(12.5%) 2(28.57%) 1(14.28%) 1(14.28%) NS
(4)Sever Pain N-% 2(25%) 3(37.5%) 3(37.5%) 2(82.57%) 2(28.57%) 2(28.57%) NS
5-Commulative succ rate 6(75%) 5(62.5%) 5(62.5%) 5(71.42%) 5(71.42%) 5(71.42%) NS
Spasmodic dysmenorrhea. N=7 Spasmodic dysmenorrhea. N=6
1-No pain
N-% 1(14.28%) 1(14.28%) 1(14.28%) 2(33.33%) 4(66.66%) 4(66.66) S
2- Minimal pain N-% 1(14.28%) 1(14.28%) 1(14.28%) 2(33.33%) 1(16.66) 1(16.66) NS
3-Tolerable pain N-% 1(14.28%) 1(14.28%) 1(14.28%) 1(16.66) 1(16.66) 1(16.66) NS
4-Sever Pain N-% 4(57.14%) 4(57.14%) 4(57.14%) 1(16.66) 0 0 S
5-Commulative succ. Rate 3(42.85%) 3(42.85% 2(28.57) 5(83.33%) 6(100%) 6(100%) S
Deep Dysparonia N=9 Deep Dysparonia N=10
(1)No pain
N-% 1(11.11%) 1(11.11%) 1(11.11%) 4(40%) 5(50%) 5(50%) S
(2) Minimal pain N-% 1(11.11%) 2(22.22%) 1(11.11%) 3(30%) 3(30%) 3(30%) NS
(3)Tolerable pain N-% 4(44.44%) 2(22.22%) 2(22.22%) 1(10%) 1(10%) 1(10%) S
(4)Sever Pain N-% 3(33.33%) 4(44.44%) 5(55.55%) 2(10%) 1(10%) 1(10%) S
Cumulative success rate 6(66.66%) 5(55.55%) 4(44.44%) 8(80%) 9(90%) 9(90%)

Discussion:
Chronic pelvic pain is commonly described as pain felt below the umbilicus which lasts for at least 6 months, it also includes dysmenorrhea and dyspareunia. Definitive diagnosis is usually by laparoscopy or laparotomy. One of the most common causes of chronic pelvic pain is endometriosis, other causes of chronic pelvic pain include pelvic inflammatory disease, pelvic congestion syndrome, and nerve entrapment, neuropathic and postsurgical pain. Treatment for chronic pelvic pain depends on the underlying cause, in some patients a cause cannot be identified. When the cause of chronic pelvic pain cannot be identified, conservative treatments will be triad includes non-steroidal anti-inflammatory drugs or oral contraceptive pill. If these medical treatments fail, conservative surgical treatment options include vaginal Uterosacral ligament resection (VUSR), uterine nerve ablation (UNA) (involving transection of the Uterosacral ligaments at their insertion into the cervix by open surgical operation, or using laparoscopy) and presacral neurectomy (PSN) (involving total removal of the presacral nerves) may be beneficial.
The 1ry aim of this work is to explore the efficacy and the safety of LUNA in relief of pain in women with chronic pelvic pain in whom diagnostic laparoscopy reveals either no pathology or mild endometriosis (AFS score ≤ 5). The 2ry aim was evaluate the patients' satisfaction from the procedure during 3,6 and 12 months follow up and to test the hypothesis that response to LUNA differs according to type of the pain by two secondary analyses: (I) Women with primary or secondary dysmenorrhea, (ii) women with deep dysparonia.
In the present study, The efficacy (that was evaluated by the percentage of women who reported no, minimal or tolerable or sever pain during the period of follow up and without hystererectomy or repeated LUNA.) was comparable between group I and group II at three , six and twelve months of follow up (P≤0.05). Also the overall success rate between group I and group II was comparable to each other as it was 75%, 75% and 66.66% versus 79.16%, 79.16% and 75% at three, six and twelve months respectively(P≤0.05). This is in agreement with the results of other studies in which LUNA was used to treat patients with chronic pelvic pain in whom laparoscopy reveal no pathology. Proctor et al.,(20), in his systematic review (Cochrane) and meta analysis including 6 RCTs (12-13,21-24) including LUNA (+/- control) versus control (control was diagnostic laparoscopy alone, conservative surgical treatment of endometriotic lesions, LPSN or LBCUV), reported that there were no significant differences overall in pain relief between women treated with LUNA and controls (women treated with diagnostic laparoscopy or conservative surgery alone) as pain relief up to 6 months (5 studies, N = 258): OR 1.15, 95% CI 0.66 to 1.99 , pain relief up to 12 months (4 studies, N = 285): OR 1.20, 95% CI 0.72 to 1.99 and pain relief up to 36 months (1 study, N = 116): OR 0.84, 95% CI 0.39 to 1.80). The review states that the effect of treatment may overlap with the placebo effect of laparoscopy, reducing differences in short-term efficacy between groups and the lack of power to detect a clinically important difference was an issue of concern in the trials with null results. The Lichten trial,(22) which reported significant differences in pain relief at both short- and long-term follow-up, used sequential allocation; concealment was described as inadequate. The Johnson trial(12) was considered by the Cochrane review authors to have adequate allocation concealment and randomization. Also, The review states that lack of sustained long-term benefit could be due to regrowth of nerves or pain signals being transferred via alternative routes and consequently, because of this last speculation ,in the present study Uterosacral nerve cauterization using bipolar electrosuergical current and then nerve transaction was used rather than any procedure alone. Palomba et al., (25), in his randomized controlled trial, studied 80 women with chronic pelvic pain treated with LUNA or VUSR (vaginal Uterosacral nerve resection) with a follow up till 12 months , There were no significant differences between the two study groups with regard to pain relief as Cure rate at 6 months: 82.5% at the LUNA group (33/40) versus 87.5% at VUSR group (35/40), p = 0.53 and Cure rate at 12 months: 75.0% at the LUNA group (27/36) versus 73.7% at VUSR group (28/38), p = 0.90. In non randomized multicenter trial of Zullo et al.,(26) included 58 women with predominant midline pelvic pain, cyclic or acyclic, persisting for more than 6 months treated with LUNA { 59% (34/58)}, or LPSN { 41% (24/58)}, with 6 months follow up period they found that there were no significant differences between the two study groups as regard to pain relief at 6 months but this study was excluded from the Cochran review as is was retrospective non randomized trial with short period of follow up , also in different case series of different authors (27-29) reported similar proportions of women with no chronic pelvic pain or pain not requiring treatment after LUNA at different period of follow up. In the present study endometriosis more than ( Society score >5) were excluded from the study as in the majority of women had endometriosis that treated with conservative laparoscopic procedure alone or with conservative medical therapy as well as with LUNA, it will be difficult to attribute their response to the LUNA alone or to the adjuvant therapy of endometriosis and this in agreement with the conclusion of different studies as that of Guyer et al., (30) and Davis et al.,(31), also In a randomized trial of 180 patients with symptomatic endometriosis, the addition of LUNA to conservative laparoscopic surgery for endometriosis did not reduce the medium- or long-term frequency and severity of recurrent dysmenorrheal(13). Another randomized study of 67 patients with chronic pelvic pain and laparoscopic evidence of endometriosis found no significant difference in pain outcome(12)
Patients' Satisfaction rate did not varied significantly between group I and group II at 3, 6, 12 months follow up, ( P≤0.05). The cumulative satisfaction rate was 75% , 75% and 70.83% versus 79.16%, 79.16% and 70.83% at 3, 6, 12 months between group I and group II respectively (P≤0.05) . This results goes hand in hand with the overall satisfaction rate in the meta analysis study of Proctor et al., (20) as they stated that there is no significant difference at the satisfaction rate or the need of additional treatment between the study and the control group among 6 RCTs they evaluated.
As regarding the effectiveness of laparoscopic Uterosacral nerve ablation (LUNA) (when compared to a control or no treatment) in treatment of primary (spasmodic) dysmenorrhea, and deep dysparonia, there was a statistically significant difference between both groups , as in case of 1ry dysmenorrheal ,the cumulative success rate was 42.85% , 42.85% and 28.57% versus 83.33%, 100% and 100% at 3, 6, 12 months between group I and group II respectively (P≥0.05) , and in case of deep dysparonia the cumulative success rate was 66.66% , 55.55% and 44.44% versus 80%, 90% and 90% at 3, 6, 12 months between group I and group II respectively (P≥0.05) , on the other hand as regarding the effectiveness of LUNA in treatment of secondary ( congestive ) dysmenorrhea there was no statistically significant difference between both groups , as The cumulative success rate was 75% , 62.50% and 62.50% versus 71.42%, 71.42% and 71.42% at 3, 6, 12 months between group I and group II respectively (P≤0.05) . The previous results was in agreement with that of the report of Proctor et al .,(20) as in his systematic review of 6 randomized controlled trials (RCTs), he reported that for women with primary dysmenorrhea, the OR for pain relief at 6 and 12 months was 0.67 (95% CI 0.17 to 2.61) and 0.10 (95% CI 0.03 to 0.03), respectively, in favor of LUNA. For women with secondary dysmenorrhea, the OR for pain relief at 6 and 12 months was 1.03 (95% CI 0.52 to 2.02) and 0.77 (95% CI 0.43 to 1.39), respectively. While Zullo et al.,(26) in his non randomized comparative study comparing LUNA versus LPSN in treatment patients with chronic pelvic pain, they found that LPSN had significantly higher efficacy than LUNA in the relief of dysmenorrhea, but the results were comparable for deep dyspareunia and pelvic pain, but In one case series(27) of 85 women, excellent or satisfactory improvement (not further defined) was reported by 76% (38/50) of women with dysmenorrhea and 80% (41/51) of women with deep dyspareunia after a mean follow-up of 19 months. In Cochrane Database of Systematic Reviews 2007(32) as regarding the treatment of primary dysmenorrhea there was some evidence of the effectiveness of laparoscopic uterine nerve ablation (LUNA) when compared to a control or no treatment. The comparison between LUNA and laparoscopic presacral neurectomy (LPSN) for primary dysmenorrhea showed no significant difference in pain relief in the short term; however, long-term LPSN was shown to be significantly more effective than LUNA. For the treatment of secondary dysmenorrhea six identified RCTs addressed endometriosis and one included women with uterine myomas. The treatment of LUNA combined with surgical treatment of endometrial implants versus surgical treatment of endometriosis alone showed that the addition of LUNA did not aid pain relief. For PSN combined with endometriosis treatment versus endometriosis treatment alone there was an overall difference in pain relief although the data suggests this may be specific to laparoscopy and for midline abdominal pain only. In the present study, as regarding, the effectiveness of the LUNA in relief or improve deep dysparonia was taken with great interest and discussion because of to my knowledge, there has been no similar report specifically on the treatment of primary deep dyspareunia by the LUNA procedure except that of Jung et al .,(33) study as they found that of this 12-month follow-up study of LUNA for treating primary deep dyspareunia, the satisfactory rates at 3 and 12 months were 66.7% and 50%, respectively , while in the other hand Vercellini et al.,(13) found no significant advantage on sexual satisfaction by the LUNA procedure. In our opinion, deep dyspareunia is very complicated in its pathogenesis, which includes both physical and psychiatric/psychologic aspects; hence a verified system comprising clarified definitions and criteria in the assessment of satisfaction or improvement is mandatory and will be very difficult to be practisized in our community and with our patients with the lack of group evaluators, including personnel who are qualified for appraising a sexologic and psychiatric/psychologic questionnaire to give more informed insight, and so these results need to be evaluated carefully in a large randomized trial before to be generalized.
In the present study, in relation to safety, as regarding intraoperative complications, there were no statistically significant difference between group I and group II concerning the occurrence of bleeding, uterine perforation ,visceral injuries, vascular injuries or conversion to open surgery (P ≤0.05), while on the other hand there were statistically significant difference between group I and group II as regarding the postoperative complications, as constipation, urinary urgency and uterine prolapsed were more frequently to occur among patients of the 2nd group(P≥ 0.05) . All of these complications were minimal and treated conservatively with no additional measures. This was in agreement with that of Yuan (2006)(2),who stated that The adverse events of PSN were significantly more common than those of LUNA. In general, LUNA is extremely safe except for a few complications reported in the literature, which might not be specifically associated with LUNA. Also Proctor et al., (20) in their mata-analysis found that Few complications were reported, in one non-randomized comparative study and one RCT, more complications were reported for LPSN than for LUNA. Constipation was reported in 0% (0/35) and 12% (4/34) of women treated with LUNA compared with 94% (31/33) and 21% (5/24) of women treated with LPSN. Urinary urgency, postoperative bleeding and painless labor were also reported in the LPSN groups but not the LUNA groups. Two case reports described a total of five woman with uterine prolapse after having LUNA; three women were young nulliparous soldiers undergoing airborne training and the other two women had a history of vaginal childbirth(31,34).In Cochrane Database of Systematic Reviews 2007(32) Adverse events were significantly more common for presacral neurectomy; however, the majority were complications such as constipation, which may spontaneously improve.
The National Institute for Health and Clinical Excellence(35) is examining laparoscopic uterine nerve ablation (LUNA) for chronic pelvic pain and will publish guidance on its safety and efficacy to the NHS in England, Wales, Scotland and Northern Ireland, This overview is based on one Cochrane systematic review and meta-analysis, one additional RCT, one non-randomized comparative study, four case series and two case reports(20,25-31,34) , they concluded that, there was some evidence for the effectiveness of LUNA when compared with controls or no treatment in women with primary dysmenorrhea, and there were no significant differences in short-term pain relief between LUNA and LPSN. However, in the long term LPSN was significantly more effective than LUNA and the authors concluded that there was insufficient evidence to recommend the use of nerve interruption in the management of dysmenorrhea, regardless of cause, and that further RCTs should be undertaken. On the other hand The European Society for Human Reproduction and Embryology (ESHRE) published a guideline for the diagnosis and treatment of endometriosis in 2005(30) The guideline states that ‘ablation of endometriotic lesions reduces endometriosis-associated pain and the smallest effect is seen in patients with minimal disease; there is no evidence that also performing LUNA is necessary’. A guideline published by the Royal College of Obstetricians and Gynecologists in October 2006 states that ‘There is no evidence that laparoscopic uterine nerve ablation is necessary when ablating endometriotic lesions and laparoscopic uterine nerve ablation by itself has no effect on dysmenorrhea associated with endometriosis’(37). So, So both uncontrolled or controlled randomized studies and the present study had proved the support for the LUNA in either complete relief or substantial reduction in chronic pelvic pain in a well selected patients.
In conclusion, Chronic pelvic pain is a complicated syndrome comprised of different types of pain, including dysmenorrhea, deep dyspareunia, and intermenstrual pain caused by different etiologies and in a great percent of patients, cause cannot be identified which make diagnosis and treatment a challenging task. Accumulating data from several randomized studies, and the present study ,we have now come to realize that LUNA can be an option in a well selected circumstances, specially for control of menstrual pain without endometriosis; however, its effectiveness may not extend to other indications, such as secondary dysmenorrhea associated with endometriosis but it considered as an option in patients without a cause in diagnostic laparoscopy. Also, preliminary experience in the treatment of primary deep dyspareunia, presenting a promising perspective yet without sufficient evidence on the management of deep dyspareunia. A randomized controlled study with an adequate number of patients is warranted.
References:
1- Zondervan KT,Yudkin PL,Vessey MP, Dawes MG, Barlow DH, and Kennedy SH.(1999): Prevalence and incidence of chronic pelvic pain in primary care: evidence from a national general practice database. Br J Obstet Gynaecol ;106:1149–55.
2- Yuan Ch-Ch (2006): Laparoscopic Uterosacral nerve ablation and chronic pelvic pain. J Chin Med Assoc. Vol 69, No 3, 101-103.
3- Reiter RC.(1990): A profile of women with chronic pelvic pain. Clin Obstet Gynecol 33:130-6.
4- Walker EA, Katon WJ, Jemelka RP, Alfrey H, Bowers M, and Stenchever MA (1989): The prevalence of chronic pelvic pain and irritable bowl syndrome in two university clinics. J Psychosomatic Obstet Gynecol ;12:65-75.
5- Renaer M.(1981): Chronic Pelvic Pain in Women, p1. Springer-Verlag: New York .
6- Richter HE, Holley RL, Chandraiah S, and Varner RE.(1998): Laparoscopic and psychologic evaluation of women with chronic pelvic pain. Int J Psychiatr Med ;28:243-53.
7- Hebbar S, and Chawla C. (2005): Role of laparoscopy in evaluation of chronic pelvic pain. J Min Access Surg ;1:116-120.
8- The LUNA Trial Collaboration (2003): A randomized controlled trial to assess the efficacy of Laparoscopic Uterosacral Nerve Ablation (LUNA) in the treatment of chronic pelvic pain: The trial protocol . BMC Womens Health. 2003; 3: 6. Published online 2003 December 8. doi: 10.1186/1472-6874-3-6.
9- Dawood MY.(1988): Nonsteroidal anti-inflammatory drugs and changing attitudes towards dysmenorrhea. Am J Med ;84:23–9.
10- Frankenhauser G. Die Bewegungenerven der Gebarmutter. Z Med Nat Wiss 1864;1:35.Qouted from Yuan Ch-Ch 2006:Laparoscopic Uterosacral nerve ablation and chronic pelvic pain.J Chin Med Assoc. Vol 69, No 3, 101-103.
11- Johnson N, Wilson M, and Farquhar C.(200): Surgical pelvic neuroablation for chronic pelvic pain. Gynaecol Endosc ;9:351–61.
12- Johnson NP, Farquhar CM, Crossley S, Yu Y, Van Peperstraten AM, Sprecher M, and Suckling J.(2004): A double-blind randomized controlled trial of laparoscopic uterine nerve ablation for women with chronic pelvic pain. BJOG ;111:950–9.
13- Vercellini P, Aimi G, Busacca M, Apolone G, Uglietti A, and Crosignani PG.(2003): Laparoscopic Uterosacral ligament resection for dysmenorrheal associated with endometriosis: results of a randomized, controlled trial. Fertil Steril ;80:310–9.
14- Khan KS, Khan SF, Nwosu CR, Dwarakanath LS, and Chien PFW.(1999): Laparoscopic Uterosacral nerve ablation in chronic pelvic pain: An overview. Gynaecological Endoscopy. ;8:257–265. doi: 10.1046/j.1365-2508.1999.00269.x.
15- Wilson ML, Farquhar CM, Sinclair OJ, and Johnson NP.(2000): Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhea. [Review] [6 refs]. Cochrane Database Syst Rev. :CD001896.
16- Stones, RW. and Mountfield, J. (2000):Interventions for treating chronic pelvic pain in women. [update of Cochrane Database Syst Rev. ;(2): CD000387 ; 10796713.]. [Review] [15 refs]. Cochrane Database Syst Rev. 2000. p. CD000387.
17- Sutton C, and Whitelaw N.(1993): Laparoscopic uterine nerve ablation for intractable dysmenorrhea. In: Sutton CDiamond MP. , editor. Endoscopic surgery for Gynaecologists. London, WB Saunders; . pp. 159–163.
18- Zelen M.(1974): The randomization and stratification of patients to clinical trials. J Chronic Dis. ;27:365–375.
19- Schulz KF, Chalmers I, Hayes RJ, and Altman DG.(1995): Empirical evidence of bias. Dimensions of methodological quality associated with estimates of treatment effects in controlled trials. JAMA. ;273:408–412. doi: 10.1001/jama.273.5.408.
20- Proctor ML, Latthe PM, and Farquhar CM, (2005) :Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhea. Cochrane Database of Systematic Reviews Issue 4: CD001896
21- Chen FP, Chang SD, and Chu KK, (1996) : Comparison of laparoscopic presacral neurectomy and laparoscopic nerve ablation for primary dysmenorrhea. Journal of Reproductive Medicine 41 (7): 463–6.
22- Lichten EM, and Bombard J. (1987) :Surgical treatment of primary dysmenorrhea with laparoscopic uterine nerve ablation. Journal of Reproductive Medicine 32: 37–41.
23- Sutton C, Pooley AS, and Jones KD, (2001): A prospective, randomized, double-blind controlled trial of laparoscopic uterine nerve ablation in the IP Overview: laparoscopic uterine nerve ablation (LUNA) for chronic pelvic pain Page 20 of 26 376 treatment of pelvic pain associated with endometriosis. Gynaecological Endoscopy 10 (4): 217–22.
24- Yen YK, Liu WM, and Yuan CC, (2001): Addition of laparoscopic uterine nerve ablation to laparoscopic bipolar coagulation of uterine vessels for women with uterine myomas and dysmenorrhea. Journal of the American Association of Gynecologic Laparoscopists 8 (4): 573–8.
25- Palomba S, Russo T, and Falbo A, (2006): Laparoscopic uterine nerve ablation versus vaginal Uterosacral ligament resection in postmenopausal women with intractable midline chronic pelvic pain: a randomized study. European Journal of Obstetrics and Gynecology 129: 84–91.
26- Zullo F, Pellicano M, and De Stefano R, (1996): Efficacy of laparoscopic pelvic denervation in central-type chronic pelvic pain: a multicenter study. Journal of Gynecological Surgery 12: 35–40.
27- Chapron C, Dubuisson JB, and Tardif D, (1998): Retroperitoneal endometriosis and pelvic pain: results of laparoscopic Uterosacral ligament resection according to the rAFS classification and histopathologic results. Journal of Gynecological Surgery 14: 51–8.
28- Papasakelariou C. (1996): Long-term results of laparoscopic Uterosacral nerve ablation. Gynaecological Endoscopy 5: 177–9.
29- Nascu PC, Vilos GA, and Ettler HC, (2006): Histopathologic findings on Uterosacral ligaments in women with chronic pelvic pain and visually normal pelvis at laparoscopy. Journal of Minimally Invasive Gynecology 13: 201–4.
30- Guyer C, Moors A, and Louden K. (2000) : An audit of conservative surgery for endometriosis in a district general hospital 1995–1998. Journal of Obstetrics and Gynaecology 20 (5): 514–16.
31- Davis GD. (1996) :Uterine prolapse after laparoscopic Uterosacral transection in nulliparous airborne trainees. Journal of Reproductive Medicine 41: 279–82.
32- Proctor ML, Latthe PM, Farquhar CM, Khan KS, and Johnson NP (2007):Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhea Cochrane Database of Systematic Reviews 2007 Issue 3 Copyright © 2007 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.
33- Juang CM, Yen MS, Horng HC, Cheng CY, Yu HC, and Chang CM.(2006): Treatment of primary deep dyspareunia with laproscopic Uterosacral nerve ablation procedure: a pilot study. J Chin Med Assoc;69:110–4.
34- Good MC, Copas PR, and Doody MC. (1992): Uterine prolapse after laparoscopic Uterosacral transection. Journal of Reproductive Medicine 37: 995–6.
35- National institute for health and clinical excellence (2007): interventional procedure overview of laparoscopic uterine nerve ablation (luna) for chronic pelvic pain', february 2007 . Available from: www.nice.org.uk/ip376overview.
36- Kennedy S, Bergqvist A, and Chapron C, (2005): ESHRE guideline for the diagnosis and treatment of endometriosis. Human Reproduction 20 (10): 2698–704.
37- Royal College of Obstetricians and Gynaecologists.(2006): The Investigation and Management of Endometriosis. Green-top guideline no. 24. London: RCOG; .






Case Report

A new treatment modality for women with chronic pelvic pain (CPP) with unknown or undetected cause.
Dr. Nasr Said. Nassar,
Consultant and Head Department of Obstetrics and Gynecology – Monira
General Hospital, Cairo , Egypt.
President of Egyptian Society of Chronic Pelvic Pain in Women

Abstract
A definitive diagnosis is not made for 61% of women with chronic pelvic pain (CPP) in women.
We suggest a new approach for managing these cases of women with chronic pelvic pain (CPP) in women, with unknown or undetected cause or without diagnosed etiology of chronic pelvic pain.
The new approach consists of three steps, First, pre- Laparoscopy (Medical treatment), work against pelvic infection, second, Diagnostic Laparoscopy revealed no pelvic abnormality, no obvious laparoscopic pathology detected, then doing, LUNA ( Laparoscopic Uterosacral - or Uterine - Nerve Ablation ). Lastly the third step, post- - Laparoscopy (Medical treatment), work against undetected pelvic congestion or endometriosis , also against the psychological aspect.
By the new treatment modality 67% of these patients have very good respond , (22%) have satisfactory results, (11%) did not satisfy; there was no big difference in her pelvic pain before and after the approach.
we recommend more accurate investigations with large number of patients.
Objective
The goal of this case report study is to evaluate a new regimen for treatment of about two thirds of cases of chronic pelvic pain (CPP) in women without known etiology.

Background
A definitive diagnosis is not made for 61% of women with chronic pelvic pain (CPP) in women.
(Medicine and Health Rhode Island > Jan 2003 > Chronic pelvic pain in women Fox, Sarah D).
We try to suggest a new modality of treatment which can help us to manage most of this group of patients.
We try to investigate a suggestive new approach which is a combination of different items, for treating the chronic pelvic pain in women with unknown cause or without diagnosed etiology.
Our aim is to try to standardizing an approach for treating most of the cases which we do not accurately know the precise cause of the disease.

Material and Methods
Prospective and randomized study performed :
* Through 2007 / 2008.
* Place : Chronic Pelvic Pain Unit , In Monira General Hospital, Governmental leading big hospital in Syda Zeinab , Cairo, Egypt.
* The patients were randomly taken i.e. they were patients came to our unit, within one week; it was the last week of November 2007.
*We exclude patients with diagnosed cause of pain, all the left female patients complaining of chronic pelvic pain with no definitive diagnosis is made, no obvious cause detected were nine patients, all of them are the candidates of our study.
The nine female patients complaining of chronic pelvic pain (the pain was below the level of the umbilicus i.e. lower abdomen and low back i.e. anatomic pelvis). The duration is more than 6 months, and failed previous medical trails to treat. The pelvic pain led to functional disability or daily physical, mental and emotional activities.
The nine female patients were as the following:
Number Age of patients Duration of pain/ months Type of pain Parity Other complains
1 18 8 Dysmenorrhea 0 Nothing
2 28 12 Dysmenorrhea 0 Primarily infertility
3 29 12 Dysmenorrhea 3 Nothing
4 32 24 Dyspareunia 2 Second. Infertility
5 35 24 Dull aching & heaviness 3 Second. Infertility
6 38 36 Dyspareunia 4 Low back pain
7 38 36 Dyspareunia 0 Nothing
8 42 36 Dysmenorrhea 0 Nothing
9 45 48 Dull aching pain & heaviness & Dysmenorrhea 3 Menorrahgia

the average duration of pain was 26 months (8, 12, 12, 24, 24, 36, 36, 36, 48 months). The average age was 33.9 years (18, 28, 29, 32, 35, 38, 38, 42, 45 years).
Four patients were severe dysmenorrehea, three patients dull aching pelvic pain, sometimes radiates to lower back and three patients complaining of severe dyspareunia.
All the patients had severe pain, enough to disturb her daily life style and led her to search for treatment.
All previous medical trials received before for treatments were failed or did not help too much.
Our suggestive proposed new approach protocol is performed for all the patients as following: 1- First step is meticulous evaluation by both a full history and a physical examination using the questionnaire of International Society of Chronic Pelvic Pain to narrow the differential diagnosis, and rule out a malignant neoplasm or significant systemic disease. 2- Results of the history and physical examination were normal, and did not reveal any cause to explain the chronic pelvic pain for the nine women patients. 3- Pelvic ultrasound and some laboratory testing e.g. CBC, blood sugar, urine analysis, liver functions tests, and renal functions tests, all were within normal findings for the nine patients. 4- Consultation of internist to exclude Irritable Bowel Syndrome ( IBS), chronic constipation, and other medical causes of Chronic Pelvic Pain . Also consultation of urologist to exclude urological causes e.g. Interstial cystitis, stones, infections.
The nine patients were completely free and no medical or urological causes for their pelvic pain were found. At this stage we started the treatment using our suggestive trial protocol for patients with chronic pelvic pain with no cause detected or with unknown etiology. The steps of our protocol we applied for the nine patients are: 1- Pre- Laparoscopy (Medical treatment): Work against pelvic infection, a- Azithromycin, ( Zithrokan capsules 500 mg) single dose 1000 mg b- Metronidazole, The most common brand name is Flagyl. The dosage is usually a single dose 2,000 mg, or alternatives. c- Vaginal cleaning with betadin once/day for three days before Laparoscopy.
2- Laparoscopy
a- Diagnostic Laparoscopy revealed no pelvic abnormality, no obvious laparoscopic pathology detected, ( note : we did not take any tissue or peritoneal fluid samples for
pathological or cytological studies) .

b- LUNA ( Laparoscopic Uterosacral - or Uterine -
Nerve Ablation ) is done for the nine patients. 3- Post- Laparoscopy (Medical treatment): start on the
second day post-operative as follow: a- Venotonic medication , treating the possible
undiagnosed pelvic congestion e.g. daflon
500mg twice / day for one month. b- Depot medroxyprogesterone , administered as 150 mg intramuscularly every month, once / month for only three months ( three injections). c- Nonsteroidal anti-inflammatory drugs ( NSAID)
if it is needed e.g.diclofenac 100 – 150 mg / day
or nimesulide (Sullied 200mg ). d- Reassurance is a very important issue in our
management, talking to the patients friendly
and explain all the details honestly to build her
self- confidence, trustable relationship.
Results: Within the first three months, post-laparoscopy follow up, visits were once every month at the time of the depot medroxyprogesterone injection. We evaluate the pelvic pain after this new approach by:
* The patient's feelings i.e. their own words which describe how the previous pain is disappear, reduced or is the same, after the new approach.
* Also the evaluation was by the reduction of frequency and dosage of the analgesic drugs used by the patients.
Six patients out of the nine patients ( 67%) have good respond, the pelvic pain is almost disappear and they return back to the normal daily physical, mental and emotional activities. The average uses of analgesics were variable from nothing to twice a week, they do not complain anymore and they do not search for further help by extra management.

Two patients out of the nine patients (22%) have satisfactory results, most of pelvic pain disappear, the average use of analgesics were variable from three to six times a week, and return back the most of normal daily physical, mental and emotional activities, they do not search for further help by extra management except modification of the dose and frequency of the analgesics.
The last patient (Number 9) (11%) did not satisfy; there was no big difference in her pelvic pain before and after the approach. At the end of the three months follow up, the new approach failure has been ascertain, we perform hysterectomy for her, uterine adenomyosis is proved by hystopathological examination, we are not sure if it was or not the hidden cause for the pelvic pain .

Discussion:

All women patients of chronic pelvic pain undergo extensive work up (history, physical examination, laboratorial, image studies and diagnostic endoscopical studies ,i.e. hysteroscopy and laparoscopy), but in many cases the etiology of the pain is unknown and the cause is not detected certainly. So their treatment is difficult.

We think that the cause of chronic pelvic pain in women which it could not be identified laparoscopically is hidden or early one of three possibilities:
• Infection (e.g. chlamydia),
• Endometriosis or
• Pelvic congestion.
The new approach designed for these cases of undetected cause of chronic pelvic pain in women is hitting all the previous common possible causes.
Conclusion
A definitive diagnosis is not made for 61% of women with chronic pelvic pain (CPP) in women. We believe that the cause could be is hidden or early infectin , congestion, or endometriosis. Our proposed treatment modality is doing diagnostic laparoscopy which revealed no obvious pelvic laparoscopic abnormality nor pathology detected, so , LUNA is done, in addition to treatment against pelvic infection , congestion and endometriosis as described . Results was as 67% of patients have good respond , 22% have satisfactory respond , 11% failed.
Although we believe that this treatment modality has been proven effectiveness but also we recommend more accurate investigations with large number of patients.