- Author: G Willy Davila, MD; Chief Editor: Michel E Rivlin, MD more...
The uterus, cervix, and adnexa share the same visceral innervation as the lower ileum, sigmoid colon, and rectum. Signals travel via the sympathetic nerves to spinal cord segments T10 through L1. Because of this shared pathway, distinguishing between pain of gynecologic and gastrointestinal origin is often difficult.
A brief summary of the causes of gynecologic pain with links to other Medscape Drugs & Diseases articles is included at the end of this article.
Acute Pelvic Pain
Associated Symptoms and Differentiation
Acute pain due to ischemia or injury to a viscus is accompanied by autonomic reflex responses such as nausea, vomiting, restlessness, and sweating. The following is a discussion of some of the important gynecologic causes of acute abdominal pain.
Culdocentesis can still be a useful diagnostic aid for differentiating the cause of acute gynecologic pain. In the absence of a positive pregnancy test result, fresh blood suggests a corpus luteum hemorrhage, old blood suggests a ruptured endometrioma (chocolate cyst), purulent fluid suggests acute pelvic inflammatory disease (PID), and sebaceous fluid indicates a dermoid cyst. However, culdocentesis has largely been superseded by imaging modalities like ultrasonography.
Due to its life-threatening nature, ectopic pregnancy must be ruled out when a reproductive age woman presents with pelivic pain and a positive pregnancy test. An unruptured ectopic pregnancy produces localized pain due to dilatation of the fallopian tube. Once the ectopic pregnancy is ruptured, the pain tends to be generalized due to peritoneal irritation. Symptoms of rectal urgency due to a mass in the pouch of Douglas may also be present. Syncope, dizziness, and orthostatic changes in blood pressure are sensitive signs of hypovolemia in these patients.
Abdominal examination findings include tenderness and guarding in the lower quadrants. Once hemoperitoneum has occurred, distension, rebound tenderness, and sluggish bowel sounds may develop.
Pelvic examination may reveal cervical motion tenderness that is exaggerated on the side of the tubal ectopia.
Initially, a sensitive serum or urine pregnancy test should be performed. Transvaginal ultrasonography should be performed. If an intrauterine gestational sac with a fetal pole is identified, the chances of a coexisting ectopic pregnancy are remote. Such a heterotopic gestation should be considered in patients taking ovulation-inducing drugs. Serial serum beta-human chorionic gonadotropin (hCG) estimations are often helpful in making the diagnosis. In early intrauterine gestations, the doubling time for hCG is usually 48 hours. Only 15% of cases are exceptions to this rule. In the absence of the availability of ultrasonography or in an emergency setting, culdocentesis can be of value to detect unclotted blood. A hematocrit of less than 16% (in the peritoneal blood) excludes hemoperitoneum.
Laparoscopy should be attempted if the patient is hemodynamically stable, a high index of suspicion remains, or the patient complains of increasing pain despite adequate analgesia.
Treatment options for an unruptured ectopic pregnancy include salpingostomy and salpingectomy. These may be performed laparoscopically or by open procedure. Laparoscopic salpingostomy has been found to be less successful than open surgery due to higher persistent trophoblastic rate. Methotrexate, a folic acid antagonist, is also used for the treatment of unruptured ectopic pregnancy, with a variable dose regimen being more successful than a single dose regimen. A ruptured ectopic pregnancy requires a laparotomy with removal of blood clots, although it can be performed via the laparoscopic route in experienced hands.
Corpus luteum hematoma
This condition develops in the luteal phase of the menstrual cycle. Slow leakage produces minimal pain. Frank hemorrhage can lead to hemoperitoneum and hypovolemic shock. Generalized abdominal pain and syncope are features of such a presentation. Treatment includes laparoscopy or laparotomy, evacuation of clots, and control of ovarian bleeding.
The most common causes are dermoid cyst, cystadenoma, and endometrioma. Because the amount of blood loss is usually minimal, hypovolemia does not supervene. Peritoneal irritation due to leakage of cyst fluid can lead to significant tenderness, rebound tenderness, abdominal distension, and hypoperistalsis. Treatment involves cyst removal.
Changes in ovarian axial morphology, which are typically secondary to ovarian cysts (most commonly dermoids), can undergo torsion around the ovarian pedicle. Frequently, torsion resolves spontaneously, and the only presenting symptom is lower abdominal pain. Persistent torsion progresses to occlusion of the venous drainage of the ovary, which leads to congestion, ovarian enlargement, thickening of the ovarian capsule, and subsequent infarction. Pain is typically colicky and eventually becomes severe and is accompanied by nausea, vomiting, and restlessness. Infarction also leads to fever and mild leukocytosis. On pelvic exam, a tender unilateral mass in the anterior pelvis may be palpable.
If the ovary appears viable based on laparoscopic examination findings, the pedicle may be untwisted and the cyst removed. An infarcted ovary must be removed.
For more information, see Adnexal Tumors.
Acute Pelvic Inflammatory Disease
Acute salpingo-oophoritis is a polymicrobial infection that is transmitted sexually. Neisseria gonorrhoeae and Chlamydia trachomatis are usually identified in patients with PID, and both organisms often coexist in the same patient. Gonococcal disease tends to have a rapid onset, while chlamydial infection has a more insidious onset. The US Centers for Disease Control and Prevention (CDC) has recommended strict diagnostic and management guidelines for the treatment of PID in an effort to reduce serious preventable sequelae such as adhesions and infertility. See the following treatment guidelines:
Diagnostic criteria for PID
All of the following criteria must be present:
Lower abdominal tenderness
Cervical motion tenderness
Diagnosis may also be supported by any of the following criteria:
Temperature greater than 101°F (38.3°C)
Abnormal cervical or vaginal discharge
Laboratory evidence of C trachomatis or N gonorrhoeae
Elevated erythrocyte sedimentation rate or elevated C-reactive protein value
Definitive criteria for diagnosis include the following:
Positive findings on transvaginal ultrasound or other imaging technique demonstrating thickened fluid-filled tubes with or without tubo-ovarian abscess or free pelvic fluid
Positive endometrial biopsy findings
Positive laparoscopy findings
Outpatient management of PID
See the list below:
Regimen B includes ceftriaxone at 250 mg IM, cefoxitin at 2 g IM plus probenecid at 1 g PO, or another parenteral third-generation cephalosporin. Add doxycycline at 100 mg PO bid for 14 days to whichever of the above is chosen. Metronidazole 500 mg bid may be added for 14 days.
Cephalosporins and quinolones are no longer recommended for treatment of infections possibly related to gonococcal infections because of the emergence of resistant strains. [3, 4, 5, 6]
Inpatient management of PID
See the list below:
Regimen A includes cefotetan at 2 g IV q12h or cefoxitin at 2 g IV q6h. Add doxycycline at 100 mg IV/PO q12h to the above choice.
Regimen B includes clindamycin at 900 mg IV q8h plus gentamicin at 2 mg/kg IV/IM loading dose followed by 1.5 mg/kg q8h as a maintenance dose.
Ampicillin/sulbactam 3 g IV q6h, plus doxycycline 100 mg IV/PO q12h.
Admission criteria for PID
See the list below:
Inability to exclude surgical emergencies such as appendicitis
Immunosuppression (including HIV infection with low CD4 count)
Confirmed or possible pelvic abscess
Intrauterine device in situ
High fever or severe nausea and vomiting
Inability to comply with an outpatient regimen
Failed outpatient therapy
Significant fertility issues
For more information, see Pelvic Inflammatory Disease.
A ruptured abscess can lead to gram-negative endotoxic shock; therefore, this condition is a surgical emergency. The most common presentation is bilateral, palpable, fixed, tender masses. Patients often present with generalized abdominal pain and rebound tenderness caused by peritoneal inflammation. In such cases, the infected tissue must be surgically removed under broad-spectrum antibiotic coverage. Preoperative antibiotic coverage for 24-48 hours is recommended if the patient is stable.
Fibroids are benign fibromuscular tumors of the uterine wall which can grow under hormonal influence – and achieve the size of an advanced gestation uterus. They frequently involute after menopause. In the interim, they can be associated with pelvic pain, abnormal (and frequently heavy) bleeding and symptoms related to pelvic pressure from the mass effect. They are the most common indication for hysterectomy in reproductive age women.
This may occur during pregnancy when rapid growth of the tumor outstrips its blood supply. This condition is conservatively managed as much as possible.
Twisted subserous fibroid
A pedunculated subserous fibroid may twist and undergo necrosis, causing acute abdominal pain. It may be removed by laparoscopy or an open procedure.
A pedunculated submucous fibroid may present with cramping pain and vaginal bleeding. Hysteroscopic resection is the treatment of choice.
Oral ulipristal acetate, a progesterone receptor modulator in the same class as mifepristone, was as effective as leuprolide acetate in controlling bleeding with fewer side effects. Fibroid shrinkage was less marked but the effect was longer lasting. Long-term changes in the endometrium have not yet been established.
Recurrent Pelvic Pain
Mittelschmerz is midcycle abdominal pain due to leakage of prostaglandin-containing follicular fluid at the time of ovulation. It is self-limited, and a theoretical concern is treatment of pain with prostaglandin synthetase inhibitors, which could prevent ovulation.
Pain associated with endometriosis may worsen premenstrually or during menses. Patients experience generalized lower abdominal tenderness, and associated complaints include dysmenorrhea, dyschezia, and dyspareunia. Endometriotic deposits in both the uterosacral ligaments and rectovaginal septum contribute to pain during intercourse. Painful defecation is due to infiltration of the bowel wall by endometriotic deposits. Importantly, remember that the pain associated with endometriosis is not correlated with the presence or amount of visible endometriotic tissue. In fact, prevalence of endometriosis is the same in women with and without pain.[8, 9] Rather, pain is related to the chemical mediators of inflammation and neural infiltration.
Ovulation suppression using different drugs has been tried in order to reduce the pain associated with endometriosis. Overall, no difference appears to exist in the efficacy of danazol, gestrinone, oral contraceptives, depot medroxyprogesterone acetate, and gonadotropin-releasing hormone (GnRH) analogs in placebo-controlled trials. However, dydrogesterone was found to be less effective. According to a Cochrane review, ovulation suppression provides no benefit in subfertile women with endometriosis who wish to conceive.
The absolute benefit for women undergoing surgical ablation of endometriosis is 30-40% over women having only diagnostic laparoscopy, in the short term. This benefit reduced over time, and reoperation rate is as high as 50%. In cases of rectovaginal endometriosis, significant short-term pain relief was reported by up to 80%, but at 1-year follow-up, 50% required analgesics or hormones for pain relief. During postoperative treatment, GnRH analogs resulted in significantly reduced pain scores in women who received treatment for 6 months. The evidence for hormone replacement therapy in women with postsurgical menopause for treatment of endometriosis is unclear at present.
Laparoscopic cystectomy of an endometrioma was found to be superior to simple drainage for treatment of recurring pain; it has been shown to result in lower recurrence of signs and symptoms of endometriomas and higher cumulative pregnancy rates.[13, 14]
GnRH agonists were used for 6 months as the only treatment in patients with documented endometriosis. At 5 years, more than half the patients were symptom-free. The best responses were obtained in patients with mild or moderate disease. Among those with persistent or recurrent pain, an increasing correlation existed with the severity of the endometriosis.
For more information, see Medscape Reference article Endometriosis.
By definition, primary dysmenorrhea is menstrual pain associated with ovulatory cycles in the absence of structural pathology. It usually manifests in younger women, and a study on the natural course of dysmenorrhea found that most women are affected throughout the menstrual years. Improvement is more likely in women who bear children. Patients experience suprapubic cramping pain that may radiate to the anterior thigh or sacral region. Pain may be accompanied by autonomic symptoms such as nausea, vomiting, and syncope. The onset of primary dysmenorrhea is a few hours prior to the onset of menses, and pain usually lasts up to 72 hours. More than 80% of patients have an excellent response to treatment with prostaglandin synthetase inhibitors. Oral contraceptives may be used with equal effectiveness in patients who desire simultaneous fertility control.
Smoking was associated with a higher relative risk of severe dysmenorrhea. In a systematic review, naproxen, ibuprofen, and mefenamic acid were more effective for pain relief compared to placebo. The Cochrane reviews have analyzed various studies and found high frequency transcutaneous electrical nerve stimulation (TENS) and acupuncture to be effective for dysmenorrhea. Laparoscopic uterine nerve ablation (LUNA) is shown to be effective for women with dysmenorrhea without endometriosis. Other drugs that have been reported with some success include nitroglycerin, terbutaline, and guaifenesin.
Secondary dysmenorrhea is cyclic menstrual pain associated with structural pathology. The most common causes are endometriosis, adenomyosis, and the presence of an intrauterine device. Pain starts 1-2 weeks prior to the onset of menses and persists for a few days after cessation of flow. Hypertonic uterine activity coupled with an excess of prostaglandins is postulated to be the cause of secondary dysmenorrhea. Patients are somewhat less responsive to nonsteroidal anti-inflammatory drugs (NSAIDs) and combination oral contraceptives compared with patients with primary dysmenorrhea. Presacral neurectomy (PSN) has been shown in a single randomized trial to improve severe dysmenorrhea due to endometriosis. A Cochrane review found presacral neurectomy to have better pain control in the long term than LUNA, albeit with adverse effects like constipation.
Adenomyosis typically manifests in women in their 40s and is essentially a clinical diagnosis. It coexists with endometriosis and fibroids, and a study found that prior uterine surgery was significantly associated with increased risk of adenomyosis. Dysmenorrhea is associated with dyspareunia, dyschezia, and acyclical uterine bleeding. The uterus is soft and tender, especially around the time of menstruation. Magnetic resonance imaging shows an enlarged junctional zone and myometrial cysts, whereas ultrasonography shows heterogenous abnormal myometrial echogenicity in patients with adenomyosis. Histopathologic correlation with the clinical diagnosis can be found in only half the cases. For reproductive-aged women, treatment includes NSAIDs, combination oral contraceptives, progesterone-only pills, levonorgestrel intrauterine contraceptive devices, and GnRH agonists. Hysterectomy is a last resort.
Chronic Pelvic Pain
Definition and Differentiation
The American College of Obstetrics and Gynecology (ACOG) defines chronic pelvic pain (CPP) as continuous or noncyclical pelvic pain of longer than 6 months duration that localizes to the anatomic pelvis, abdominal wall at or below the umbilicus, lumbosacral back, or the buttocks and is of sufficient severity to cause functional disability or lead to medical care. Nearly 4% of women are thought to have ongoing CPP. It forms the indication for 18% of all hysterectomies and 40% of gynecologic laparoscopies. Even the relationship of recurrent pain to menstruation or the presence of dyspareunia is only suggestive.
Annually, 400,000 laparoscopies are performed on patients with endometriosis and chronic pelvic pain. Negative laparoscopic findings occur in 40% of patients.
Important nongynecologic causes that must be considered in the differential diagnosis include irritable bowel syndrome (IBS), interstitial cystitis (IC), and pelvic floor myofascial syndrome. Importantly, rule out abdominal wall etiologies that are aggravated by raising of the head or raising of straightened legs while supine.
For more information, see Medscape Reference article Chronic Pelvic Pain in Women.
Dyspareunia as a Significant Factor
Patients with deep, internal, or thrust dyspareunia often express a feeling that some sort of internal collision is occurring during sexual activity. Any pelvic pathology may be responsible for this discomfort, but abnormalities such as endometriosis, pelvic adhesions, pelvic relaxation, malposition (retroversion), adnexal pathology or prolapse, and uterine fibroids are the most likely causes. IC may cause dyspareunia before it proceeds to chronic unremitting pain. IBS may also cause dyspareunia and pain at the apex of the vagina.
A study using conscious pain mapping during awake laparoscopy found that peritoneal adhesions and filmy adhesions that allowed for movement between 2 structures had the highest pain scores, while dense, fixed adhesions caused less pain. Pain is acyclical and not accompanied by vaginal bleeding. Dyspareunia and symptoms suggestive of intermittent subacute bowel obstruction may be associated with adhesions. Adhesiolysis should be recommended with realistic expectations, and a multidisciplinary approach in a pain clinic may be worthwhile prior to attempting surgery. In one study, cure or improvement was reported in two thirds of patients with chronic pelvic pain and nearly half of those with dysmenorrhea.
In a randomized study, patients with severe adhesions involving the intestinal tract were shown to benefit from adhesiolysis. A study found adhesions deflecting the sigmoid colon to the pelvic sidewall in 38% of patients with chronic pelvic pain. Among patients without detectable endometriosis, 80% had a significant reduction in symptoms after adhesiolysis on an 18-month follow-up. Various agents have been reported to reduce adhesion formation, but none have gained universal acceptance. A small randomized study of 25 patients found a significant improvement in right-sided pain in women who underwent paracolic adhesiolysis.
The issue of prevention of adhesions after pelvic surgery has been an important one. In a Cochrane review, the authors found that Interceed was the only agent that prevented new adhesion formation and reformation following laparoscopic surgery or laparotomy. However, its use did not lead to an improvement in pregnancy rates.
Chronic Pelvic Inflammatory Disease
Pain is thought to be due to infection or adhesions that exacerbate the baseline condition. However, a animal study failed to show adhesions following direct bacterial inoculation. Infection may be accompanied by fever, leukocytosis, and gonococcal or chlamydial infection. Laparoscopy and peritoneal fluid cultures help confirm the diagnosis in most cases. Empiric treatment with antibiotics should be commenced prior to laparoscopy.
Ovarian Remnant Syndrome
Following a total abdominal hysterectomy and bilateral salpingo-oophorectomy, the ovarian remnant can undergo cystic changes that cause pain. Hormonal suppression with danazol, combined oral contraceptive pills, high-dose progestins, and GnRH agonists are possible treatment options. Diagnosis may be aided by ultrasonography. Finding the ovarian tissue may be challenging. As with all laparoscopic surgery, operator expertise is vital in the success of the procedure, because of the dense adhesions that are often present. Otherwise, a laparotomy maybe indicated.
Irritable Bowel Syndrome
IBS is one of the most common functional intestinal disorders. It is defined as a group of functional disorders in which abdominal discomfort or pain is associated with defecation or a change in bowel habits. IBS also involves features of disordered defecation.
Rome criteria for IBS
Recurrent symptoms (2 of 3) present for at least 12 weeks in the preceding year
Abdominal pain relieved with defecation
Onset associated with change in frequency of stool
Onset associated with change in stool appearance
Symptoms supportive of diagnosis
Abnormal stool frequency
Abnormal stool form
Abnormal stool passage
Passage of mucus
History plays an important role in excluding causes such as lactose intolerance, which present with similar symptoms. Upon examination, a tender sigmoid colon is often palpable. Fiber supplementation has not been shown to have significant benefits and should be reserved for patients with hard stools. Patients with recurrent severe abdominal cramps may benefit from antispasmodics such as dicyclomine and hyoscyamine, although this treatment has not been substantiated in controlled studies. Patients with severe IBS need a multifaceted approach that includes psychiatric evaluation because symptoms may be a part of a somatization disorder.
Low-dose antidepressants such as amitriptyline and selective serotonin reuptake inhibitors may have an adjunctive role. Alosetron (Lotronex) has been reintroduced to the US market and is approved for severe chronic diarrhea-predominant IBS, but only after other treatment modalities are unsuccessful, because of the risk of serious adverse gastrointestinal events (eg, ischemic colitis, serious complications of constipation). These adverse effects have resulted in hospitalization, blood transfusion, surgery, and death.
Tegaserod (Zelnorm), which is a partial agonist of the 5-hydroxytryptamine receptor that helps symptoms of IBS, alleviates constipation and accelerates intestinal transit. A meta-analysis found tegaserod to have significant benefits in women with constipation-predominant IBS.
Tegaserod was withdrawn from the US market in March 2007 due to an excess number of serious cardiovascular adverse events, including angina, myocardial infarction, and stroke.
Linaclotide (Linzess) was recently approved for constipation-predominant IBS and has proven particularly useful in women.
For more information, see the FDA MedWatch Product Safety Alert.
Loperamide was also found to be useful for women with painless diarrhea. It is now available on the US market. Fedotozine (investigational in the United States) is a kappa-opioid agonist that decreases intestinal hypersensitivity and may help decrease bloating pain. Substance P antagonists are currently being evaluated for the treatment of IBS. Patient support groups can also be useful.
Approximately 60% of patients with chronic pelvic pain may have IBS as a primary or coexistent diagnosis. The Rome criteria for diagnosis should be used in routine clinical practice. Early diagnosis allows the formulation of a management plan that includes counseling and nonpharmacologic interventions, which play important roles in alleviating patient symptoms.
Myofascial etiologies occur in 15% of patients with chronic pelvic pain. Trigger points should be searched for during a methodical abdominal wall and pelvic examination, as they are hyperirritable spots usually within a taut band of skeletal muscle or in muscle fascia. These are focally painful upon compression and can give rise to characteristic referred pain, tenderness, and autonomic phenomena. Women may experience pain from trigger points (areas overlying muscles that induce spasm and pain) in the myofascial layers of the pelvic sidewall or pelvic floor. The obturator internus and levator ani are common sites and should be palpated. A study found levator pain in 87% of women with diagnosed interstitial cystitis (IC). Coexisting symptoms, such as frequent headaches, nonrestorative sleep, diffuse tender points, and fatigue, may be suggestive of systemic disorders such as fibromyalgia.
Treatment for trigger points usually involves hyperstimulation analgesia (eg, stretching, cold spray), local injection of anesthetic agents, TENS, and acupuncture. All of these treatments act as counterirritants that alter the central gate or threshold control and result in the prolonged response. The action of an injected local anesthetic has the effect of blocking the central response. A small study of 18 women found improvement in 72% with trigger point injections combining anesthetic agents and triamcinolone. A randomized placebo-controlled trial from Australia found significant improvements in nonmenstrual pelvic pain and pelvic floor spasms in women treated with botulinum toxin type A.
Myofascial pain may manifest as focal lower abdominal pain due to entrapment of the genitofemoral or ilioinguinal nerves, which is a sequela of Pfannenstiel incisions. A bupivacaine nerve block is both a diagnostic and therapeutic measure. Cryoneurolysis or surgical removal of the involved nerve should be reserved for recalcitrant cases. Manual therapy of pelvic floor myofascial trigger points is also reported to improve pain in women with IC and in women with frequency-urgency syndrome.
Considerable overlap exists in symptomatology in patients with IC and IBS. Although some authorities believe that the National Institute of Diabetes and Digestive and Kidney Diseases criteria are too rigid, the criteria still serve as a useful clinical guide for understanding the complex nature of the problem.
See the list below:
Hunner ulcer or diffuse glomerulations (ie, small bleeding points on the bladder surface seen after hydrodistension of the bladder)
Pain associated with the bladder or urinary urgency
See the list below:
Age younger than 18 years
Duration of symptoms less than 9 months
Urinary frequency fewer than 8 times per day
Absence of nocturia
Benign or malignant tumors
Active herpes infection
Bladder or lower ureteric calculi
Involuntary bladder contractions
Bladder capacity less than 350 mL while awake
Symptoms relieved by antibiotics, urinary antiseptics, analgesics, anticholinergics, or muscle relaxants
Cystoscopic evaluation under anesthesia can be particularly useful, although not required for the diagnosis to be made. Bladder distention to anesthetic capacity (volume where spontaneous fill stops while patient is under anesthesia) will frequently demonstrate a restricted bladder capacity, and the presence of petechiae and glomerulations on the bladder wall upon bladder re-fill suggest the presence of IC. Biopsy can be performed to identify the presence of plasma cells within the bladder wall – pathologists must be asked to perform a specific Giemsa stain on the specimen in order to identify these cells.
Interestingly, patients frequently report symptom improvement after hydrodilation under anesthesia for period of up to 6 months. It is thought to be due to interruption of the gap junctions in the bladder wall.
A study found evidence of IC on cystoscopy findings in 38% of patients who underwent laparoscopy for chronic pelvic pain. In a longitudinal study of a cohort of IC patients, the most common sites of pain were lower abdominal (80%), urethral (74%), and lower back (65%).
Two different etiologic mechanisms have been suggested for IC. The classic or ulcerative variant is inflammatory in origin, and the nonulcer variant is neuropathic in origin. This has implications for choice of therapy. An evidence-based therapeutic algorithm for treatment does not exist.
Hydroxyzine is a histamine receptor antagonist with effects on the central and peripheral nervous systems. Hydroxyzine is suggested to have a good clinical effect in patients with IC. The dose is 25-50 mg bid for 14 days.
Amitriptyline is a tricyclic antidepressant that also blocks the H1 histamine receptor. Amitriptyline acts via blockade of acetylcholine receptors, including inhibition of reuptake of released serotonin and norepinephrine. It also has a sedating action via the H1 receptors. A placebo-controlled, randomized trial showed significant improvement in patients with IC who were treated with amitriptyline.
Corticosteroids are not widely used because of adverse effects such as fluid retention and osteoporosis. However, a study reported improved pain control and overall satisfaction with oral prednisone in a cohort of women with severe refractory IC.
Pentosan polysulfate sodium (PPS) (Elmiron) is claimed to restore the depletion in the glycosaminoglycan (GAG) layer. A double-blind placebo-controlled trial revealed subjective improvements in pain, urgency, frequency, and nocturia. Patients also demonstrated objective improvement in average voided volume. However, no objective demonstration of improvement was noted in urinary frequency. Another study found that the classic subtype of IC responds better than the nonulcer form. In a placebo-controlled trial, one quarter of the patients reported more than 25% improvement. A good response is expected after 4-12 months of treatment, and 50% of patients demonstrate improvement in this time. The dose is 150-200 mg bid between meals. A later study evaluating PPS and hydroxyzine failed to show improvement in most women. Chondroitin sulfate is another drug that replenishes the GAG layer. The dose is 50 mL twice a week, then decreasing to once weekly for 4 weeks. Remission is maintained with monthly instillations.
Intravesical instillation therapy can be performed using agents that are cytoprotective or cytodestructive. Cytoprotective agents include heparin, which may be given in a dose of 20,000 IU in 10 mL of sterile water. Some authors have used methylprednisolone in combination with heparin. A combination of heparin with alkalinized lidocaine was shown to provide better symptom relief than heparin alone.
Cytodestructive agents include dimethyl sulfoxide (DMSO), silver nitrate, and bacille Calmette-Guérin (BCG) vaccine. DMSO is a scavenger for intracellular hydroxy free radicals. It is an anti-inflammatory agent and a local anesthetic. It is instilled twice as 50 mL of 50% solution. It may be given with a cocktail of gentamicin, lidocaine, sodium bicarbonate, and heparin. DMSO provides relief in about two thirds of cases, and it increases bladder compliance and inhibits detrusor contractions. BCG is thought to modulate immune responses. It is instilled as 12.5 mg (50 mL) weekly for 4-6 weeks. A placebo-controlled trial failed to show significant benefit with BCG.
Capsaicin is another drug that has been successful in patients with IC. Capsaicin is a selective neurotoxin for small myelinated class C afferent neurons. It reflexly inhibits bladder contractions, decreases their amplitude, and increases the residual volume. Patients with urgency and frequency due to idiopathic diabetes insipidus or sensory urgency have not responded as well to capsaicin. Also, 40 mL of 2% lidocaine is given to effect anesthesia from the initial excitation. The dose of capsaicin is 50 mL instilled over a 4-week period. Approximately 44% patients were content with this treatment, and an additional 36% had a decrease in the frequency of urge incontinence. Capsaicin requires reinstallation after 6 months.
Resiniferatoxin is an agent that works on a similar principle. A study showed it to be a promising agent for the treatment of IC.
A Cochrane review of intravesical treatments for IC found that the evidence was most promising for BCG and oxybutynin.
Cystectomy and ileal conduit was the most frequently used major surgical procedure. A review of prescribed treatments in the IC database revealed that cystoscopy with hydrodistension is the most popular treatment. Sacral neuromodulation, hyperbaric oxygen, botulinum toxin (BTX-A), and cyclosporine A are among the newer modalities in the treatment of IC and have been tried with some success. Long-term results are needed before these should be recommended as primary measures.
Urethral Syndrome and Trigonitis
Patients with urethral syndrome or trigonitis present with classic symptoms of urinary tract infection, but urinary culture results are negative for infection. Symptoms include frequency, urgency, and pressure in the absence of nocturia. Physical examination reveals a tender ropelike urethra, or a focally tender trigone. The clinical course is marked by remissions and exacerbations. Causes include chlamydia, mycoplasma, herpes simplex, urethral trauma, atrophy, stenosis, and functional obstruction. Female prostatitis is believed to be due to inflammation of the paraurethral glands and is believed to be a frequent cause of urethral syndrome. There is typically a history of an initiating UTI – frequently having gone untreated for a significant period of time. Clinical examination reveals localization of tenderness to these glands. Treatment of urethral syndrome/trigonitis should be tailored to the individual cause. Patients with sterile pyuria respond to a 2- to 3-week course of doxycycline or erythromycin. The course has to be repeated in many patients. All postmenopausal women should also receive a trial of local estrogen therapy. Urethral dilatation and biofeedback have been used for resistant cases.
Posthysterectomy syndrome is pain due to a low-grade cuff cellulitis, seroma or hematoma of the cuff, or neuralgia related to transection of the nerve tissue. Resection of a portion of the vaginal cuff occasionally helps relieve the pain.
Hysterectomy for Chronic Pelvic Pain
Long-term studies have shown that success with hysterectomy is disappointing when the only indication is pain. If the pain has persisted for more than 6 months, has not responded to analgesics, and is causing significant distress and impairment, then hysterectomy may be considered an option after counseling the patient that the pain may persist after surgery.
Newer treatment modalities like percutaneous tibial nerve stimulation have shown initial promise. Because of their noninvasive nature, they are likely to be tried in women with unexplained pelvic pain.
Vulvar pain can be challenging in both diagnosis and management. This section utilizes the Consensus Terminology and Classification of Persistent Vulvar Pain and Vulvodynia as a basic template. Some of the terminology used here is redacted from that scholarly document and others.[50, 51] The clinician should be aware that there are multiple and diverse etiologies for vulvar pain including vulvodynia, infections, neoplasms, neuropathies, inflammatory dermatoses, post-traumatic, hormonal, environmental exposures and other causes. Co-morbidities are common. One must avoid a premature diagnosis of a psychological, psychosomatic origin.
This is probably the most enigmatic cause of vulvar pain. Defined as persistent vulvar pain for over 3 months with no other discernable cause, it may affect up to 8-9% of women at some point in their lives. It can be primary, or secondary to another vulvar disorder, and frequently presents with severe dyspareunia. It is often seen as an erythematous and tender area of the mucosa in the posterior vestibule (fossa navicularis and fourchette), but sometimes the affected area looks normal. Patients often describe their pain as burning, sharp, cutting, and “broken glass.” Vulvodynia can be localized, (such as that described above) generalized, or mixed. Provoked vulvodynia (most often with intercourse or clothing contact) or spontaneous is recognized, and the temporality varies widely (immediately with contact, or delayed). Severity of vulvodynia ranges from mild to disabling. Vulvodynia is not responsive to steroids. Treatment may include topical or systemic gabapentin or pregabalin, tricyclics such as amitriptyline, and other medications. Physical therapy and biofeedback have shown success with selected cases. In refractory cases, surgery is a viable option with a reported high degree of success. Further support, insights, and advice for patients is available through the National Vulvodynia Association (nva.org).Clitorodynia is a special situation because of the emotional impact involved. It is essential to avoid dismissing vulvodynia and other causes of vulvar pain (see below) as sexual aversion or other psychological disorder without a diligent search for a medical cause. Referral to a colleague familiar with vulvar pain should be employed in cases where any doubt exists Sexual phobias are relatively infrequent, and relationships can be destroyed through inaccurate diagnosis.
Candida spp . infections, when persistent, recurrent, and tissue-invasive are the most frequent microbial etiology of vulvar pain. In addition to C. albicans, several other species can be causative. They include C. glabrata, C. tropicalis, C. parapsilosis and others. Signs and symptoms are different from those seen with albicans - more burning pain and no “cottage-cheese” discharge. History and examination can be aided by microscopy and polymerase chain reaction (PCR) testing in diagnosing what can be very elusive diagnoses. Candida urinary tract infections can occur, and prostatic infection in male partners is a possible, albeit infrequent vector. With emerging fluconazole resistance, other candidacidal agents may be necessary, and probably should be prescribed by an experienced provider. Herpes (HSV1 or HSV2) is not at all uncommon. At times the evanescent shallow ulcerations (excoriations) may be not be recognized by the patient and episodic pain is the only complaint. The typical evaluation includes history, examination during an outbreak, and cultures or PCR testing. Treatment includes acyclovir, famciclovir and valacyclovir for acute cases and for longer term prophylaxis. Prevention of secondary infection is also important. Bacterial infections can also be quite painful. Those include Streptococcus, and MRSA. Colon-based organisms may at times be problematic, especially in patients with fistulae, and/or Crohn’s Disease. Clinicians should also be aware vaginal infections can results in vulvar pain, secondary to an irritating vaginal discharge. A yellow or greenish hue, especially in a malodorous purulent discharge is a strong indicator of bacterial infection and/or STD. Microscopy and pH, done easily in a clinical setting, is helpful: excess WBCs (usually in similar ratio to epithelial cells) and a high pH suggest bacterial infection. Normal WBC presence with low pH is more compatible with Candida. Cultures, PCRs, are useful but are not absolutely confirmatory. Candida spp. are seen via microscopy in a varying percentage of cases but false negatives are common. As always, clinical judgement is a critical component of diagnosis and treatment. Bartholin gland infection with or without abscess is a relatively common cause of vulvar pain. The tender, often warm, cystic masses at 5:00 and 7:00 on the vaginal introitus are well known by most providers.
Lichen sclerosus (LS), although infrequent, is a common inflammatory condition seen in vulvar clinics. It can be identified by the thin, white tissue seen on vestibular mucosa, as well as on keratinized skin, including perineum and perianal skin. It sometimes appears red and inflamed. LS is very pruritic, and as the disease advances the pathology worsens, resulting in pain, introital stenosis, and dyspareunia.(5) LS can be complicated by infection – usually Candida. A vulvar malignancy - differentiated vulvar intraepithelial neoplasia (d-VIN) can develop, usually in chronic, untreated cases. The malignant behavior of d-VIN is more aggressive than the more common HPV-related VIN, and therefore expert evaluation should be sought in any suspicious cases. Biopsy should be considered with or without vulvoscopy. First line treatment of LS consists of primarily powerful corticosteroids, predominantly clobetasol, in gradually declining dosage. Estrogen will help if there is coexisting atrophy, but testosterone is not nearly as effective as corticosteroids and is no longer recommended as first line treatment.[54, 55] Lichen planus (LP) is a very painful disorder. Findings consist of red, sharply-marginated lesions, erosions, and sometimes include the white, lacy patterns known as Wickham’s striae. In contrast to LS, LP can involve the vagina. With vaginal involvement, wide areas of mucosal ulceration, scarring, and a purulent discharge are common. LP also can involve other mucocutaneous sites such as gingivae and tongue. Cutaneous forms are seen is multiple skin locations. A history of extragenital LP can facilitate the diagnosis, but when in doubt, biopsy with or without vulvoscopy is called for. Successful management of LP can be formidably challenging. High potency topical or intralesional corticosteroids are initial choices[54, 55] with the calcineurin inhibitors tacrolimus 0.1% or pimecrolimus 0.1% as additional therapy in difficult cases. Generally, ointments are more effective and better tolerated. In more severe and resistant cases, as well as with multisystem involvement, systemic corticosteroids, methotrexate, azathioprine, and especially the newer biological agents can be effective. Examples are adalimumab and infliximab. Strict attention to hygiene, use of loose fitting clothing are requisite. Common substances such as vegetable oil can be soothing. Lichen simplex chronicus is a maddeningly pruritic lesion, seen mainly on keratinized skin, much like eczema. It only becomes painful when purposeful or inadvertent scratching causes excoriations that become infected. Other painful vulvar inflammations such as bullous pemphigoid, Pemphigus vulgaris, and plasma cell vulvitis are less frequently seen disorders, and can often present very challenging diagnoses. In the absence of a history of extragenital conditions, a biopsy is usually necessary. Assessment and management is augmented by the assistance of a dermatologist. A difficult inflammatory condition, often confused with infection, is Hidradenitis suppurativa. It presents in varying degrees (Hurley Stages) and results in relapsing painful abscesses and draining sinuses. The etiology is not poor hygiene. Genetic predisposition, obesity, smoking, and androgenic hormonal factors are thought to be contributory. It can also occur in the axillae, and other intertriginous areas. This chronic relapsing condition of can be devastating to the patient with in later stages, embarrassment and self-consciousness preventing sexual relations. Management includes reduction of androgenic stimulation, topical and sometimes systemic clindamycin for the anti-inflammatory effects (other antibiotics are usually not employed), zinc, and varying surgical procedures depending on the severity of the disease.
Neurologic and Muscular
Some of more challenging causes of vulvar pain include Post herpetic (H. zoster) neuropathy. The pain is episodic and a history of zoster in corresponding dermatomes is helpful for diagnosis. Probably this is more common than reported. Acute recurrences are usually very painful. Treatment consists of anti-viral and anti-seizure medications, rest, and loose clothing. Analgesics, including opiates, are often needed. Lumbosacral spine disorders can cause vulvar pain, especially if disease involves the 2nd, 3rd, and 4th sacral segments. The mechanism is neuropathic. Pudendal nerve disorders are relatively common, especially following some form of pelvic trauma, such as mechanical injury and surgery. The pain is more dull and aching than with cutaneous disorders. A history of onset following trauma, increased pain on sitting but less pain when sitting on a commode, as well as tenderness on deep palpation of the region of Alcock’s Canal are diagnostic clues. The syndrome usually arises from entrapment and compression in Alcock’s canal or other paths that the nerve travels. Neuromas are far less common. MRI scans rarely provide help with diagnosis. In some cases, clinical diagnosis is aided by abnormal perineal electrophysiologic studies, increased sacral evoked potentials latencies with abnormal “wink reflex” (clitoral compression causing anal sphincter reflex contraction), and nerve studies on the pudendal nerve. Treatment can include image-guided pudendal block (best administered by a pain management specialist who is specifically familiar with those procedures. Physical therapy can also be helpful. Muscle spasms of the obturator, perianal, and other pelvic muscles are additional causes of vulvar and vaginal pain, and are best managed by muscle relaxants, warm baths, and physical therapy. High tone pelvic floor disorders, including vaginismus , are more common types of muscle tonus disorders and demonstrate continuous dull aching pain which can be debilitating. Vaginismus typically causes a severe deep muscle pain a few centimeters within the introitus. It is provoked by intromission or tampon insertion. Both syndromes can be comorbidities of any source of pelvic pain, especially vulvodynia. Treatment modalities vary widely and employ physical therapy, administration of compounded vaginal diazepam or baclofen, and more recently botulinum toxin injections have been shown to have a rapid and sustained degree of relief. They should only be given by experienced clinicians, in part because occasional complications and side effects need to be recognized and managed expertly.
Plain (HPV-related) VIN, d-VIN, Paget’s Disease, and invasive malignancies of any histopathology can cause vulvar pain. Biopsies are always recommended if there is malignancy in the differential diagnosis. Oncologic management along with analgesics are the clear methods of treatment.
As mentioned earlier, several neuromuscular problems are secondary to obstetrical, surgical, and personal injury trauma. An additional soft tissue cause of pelvic pain, especially dyspareunia, can be dense scarring. Pulling and stretching of unyielding scars can be fairly simple to recognize, especially in the context of obstetrical trauma, surgical procedures, or personal injury. In this category, one may include radiation damage, for it is indeed a type of trauma. In cases of gynecologic, intestinal, and anal cancers, post-radiation atrophy, sclerosis, and scarring are very symptomatic. Dyspareunia is prominent. Treatment is difficult and may include vaginal dilators, emollient skin moisturizers, and physical therapy, and counseling.
It has long been known that there are innumerable soaps, bath salts, laundry detergents, fabric softeners, and such, which can result in contact irritant dermatitis.  Diagnosis of the erythematous and often painful skin lesions can be elusive because they may closely resemble other inflammatory and infectious causes of vulvar pain. An exhaustive search for the offending substance is sometimes needed, and that may be best handled by an allergist. Urinary incontinence, sometimes unreported, can also be responsible for contact dermatitis. A detailed history along with a 1-2 day phenazopyridine (Pyridium) test can be employed, looking for orange staining of a sanitary pad. Correction of incontinence, along with warm rinsing and a skin protectant are management strategies. Diaper dermatitis can develop in a remarkably short time when skin is exposed to fecal material. Discussion can be awkward but should not be deferred. Allergic dermatitis (e.g. latex) may also occur with attendant itching and pain. Again, an allergist is an important team member.
Behavioral and Psychological
Behavioral and psychological causes of vulvar pain require careful, appropriate questioning, perhaps with the assistance of a clinical psychologist. High tone pelvic floor disorders are frequently associated with sexual dysfunction. Neuroses include obsessive/compulsive washing, often with harsh soaps not intended for delicate tissues, trichotillomania, and confabulation. Psychiatric patients may have delusional stories to tell. Sexual dysfunction, can be, either primary, or secondary to most of the aforementioned pelvic pain diagnoses. Pain can be a result of sexual activity in the face of sexual aversion and phobia. Those dysfunctions can be attributable to aberrant childhood raising, dysmorphic body imaging, and physical/sexual abuse in childhood and/or adult life. Patient safety must be assured because abuse may be ongoing. Post-abuse may be regarded as a type of PTSD. These “hot-button topics” require extreme sensitivity, as well as experience. Placement of brochures and questionnaires in women’s bathrooms are a good tool. Clinical sex counsellors and therapists, psychologists and psychiatrists are essential members of the team in this context. Repeat caution: do not jump to a faulty diagnosis of sexual dysfunction until all possible organic causes of pelvic pain have been ruled out. Sexual aversions may be secondary to organic disorders, so it is imperative to be vigilant for co-morbidities.
Vulvar pain has many widely diverse etiologies. Co-morbidities are common. Many conditions closely resemble others, thus careful evaluation is advised. Biopsy should be employed in uncertain cases and if malignancy is suspected. Other healthcare professionals should be part of the team. They include psychologists, marriage counsellors, physical therapists, neurologists, pain management specialists, allergists, dermatologists, urologists, oncologists, and infectious disease specialists. A special cause of vulvar pain is vulvodynia – a complex condition lacking any uniformly successful treatment. Although sexual dysfunction can be a primary cause of pain, the diagnosis should be reserved for clear-cut cases in the absence of a purely organic cause. Consultation with specialists expertly familiar with vulvar disorders is recommended if the practitioner is not fully comfortable with these disorders.
Pain Due to Complications of Gynecologic Surgery
Thermal bowel injury is a serious complication of surgery. It occurs in 0.5-3.2 per 1000 cases, and symptoms may not develop for days or weeks. Patient presentation includes bilateral lower quadrant pain, tenderness, fever, leukocytosis, and peritonitis. Ileus or free gas under the diaphragm may be noted on a plain abdominal radiograph.
Peritonitis may occur as a consequence of undetected bowel perforations. Other complications include abscess, enterocutaneous fistula, and septic shock.
Thermal injury to the bladder or ureter may manifest up to 14 days postoperatively with abdominal or flank pain, fever, and peritonitis. Findings from an intervenous pyelogram demonstrate extravasation of urine or urinoma. Patients with mechanical obstruction may present in 1 week with a similar clinical picture.
Incisional herniae rarely become incarcerated. Patients present with abdominal pain and signs of bowel obstruction or perforation.
Hysteroscopy can result in uterine perforation especially in elderly women, which may involve the bowel. Such a possibility should be kept in mind when evaluating a patient.
Following a vaginal hysterectomy, patients may present with pelvic pain due to vaginal cuff hematoma, cellulitis, or ovarian abscess. Wound complications such as dehiscence, renal angle pain due to ureteric injury, and retention should be considered.
Osteitis pubis is a possibility in patients who undergo a Marshall-Marchetti-Krantz procedure. Operations for vaginal prolapse and urinary incontinence that use synthetic mesh can lead to the development of pelvic pain due to mesh infection, exposure through the vaginal mucosa and/or contraction and band formation during the healing process. These complications have led to removal of many mesh products from the market, but patients may present with the above symptoms many years after mesh implantation. Removal of the mesh can be performed with meticulous dissection to avoid bladder or rectal trauma, and most frequently results in improvement or resolution of the pain.
Causes of gynecologic pain can be summarized as follows:
Acute pelvic pain
See the list below:
Recurrent pelvic pain
See the list below:
- Gastroenteritis (see Gastroenteritis, Bacterial and Gastroenteritis, Viral)
- Appendicitis (see Appendicitis)
- Bowel obstruction (see Obstruction, Small Bowel)
- Diverticulitis (see Diverticulitis)
- Inflammatory bowel disease (see Inflammatory Bowel Disease)
- Irritable bowel syndrome (see Irritable Bowel Syndrome)
- Mesenteric ischemia (see Mesenteric Artery Ischemia)
- Abdominal wall
- Strangulated or incarcerated hernia (see Abdominal Hernias)
Chronic pelvic pain
See the list below:
- Inflammatory conditions
- Chronic urinary tract infection (see Urinary Tract Infection, Females)
- Overactive bladder
- Interstitial cystitis (see Interstitial Cystitis)
- Bladder stones (see Bladder Stones)
- Suburethral diverticulitis (see Urethral Diverticulum)
- Urethral syndrome (see Urethral Syndrome)
- Trigonitis (see Trigonitis)
- Constipation (very common in elderly persons) (see Constipation)
- Diverticular disease
- Inflammatory bowel disease (see Inflammatory Bowel Disease)
- Irritable bowel syndrome (see Irritable Bowel Syndrome)
- Chronic appendicitis (see Appendicitis)
- Cholelithiasis (see Cholelithiasis)
- Disk problems
- Degenerative joint disease
- Fibromyositis (see Fibromyalgia)
- Herpes zoster (see Herpes Zoster)
- Lower back pain (see Mechanical Low Back Pain)
- Levator ani syndrome (pelvic floor spasm)
- Myofascial pain (see Myofascial Pain)
- Nerve entrapment syndromes (see Nerve Entrapment Syndromes)
- Osteoporosis (see Osteoporosis)
- Posture-related pain
- Scoliosis (see Scoliosis), lordosis, kyphosis
- Strains, sprains
- Physical or sexual abuse, prior or current (see Domestic Violence)
- Lead or mercury toxicity (see Toxicity, Lead and Toxicity Mercury)
- Hyperparathyroidism (see Hyperparathyroidism)
- Porphyria (see Porphyria, Acute Intermittent)
- Somatization disorders (see Somatoform Disorders)
- Substance abuse, ie, cocaine (see Substance Abuse)
- Sickle cell disease (see Sickle Cell Anemia)
- Sympathetic dystrophy
- Tabes dorsalis
Jones HW, Jones GS. Pelvic pain and dysmenorrhea. Berek JS, Adashi EY, Hillard PA, eds. Novak's Textbook of Gynecology. 12th ed. Baltimore, Md: Williams & Wilkins; 1996: 399-428.
Hajenius PJ, Mol F, Mol BW, Bossuyt PM, Ankum WM, van der Veen F. Interventions for tubal ectopic pregnancy. Cochrane Database Syst Rev. 2007 Jan 24. CD000324. [Medline].
Update to CDC's Sexually transmitted diseases treatment guidelines, 2010: oral cephalosporins no longer a recommended treatment for gonococcal infections. MMWR Morb Mortal Wkly Rep. 2012 Aug 10. 61(31):590-4. [Medline]. [Full Text].
Centers for Disease Control and Prevention. Cephalosporin-Resistant Neisseria Gonorrhoeae Public Health Response Plan. August 2012. [Full Text].
Donnez J, Tatarchuk TF, Bouchard P, et al. Ulipristal acetate versus placebo for fibroid treatment before surgery. N Engl J Med. 2012 Feb 2. 366(5):409-20. [Medline].
Kresch AJ, Seifer DB, Sachs LB, Barrese I. Laparoscopy in 100 women with chronic pelvic pain. Obstet Gynecol. 1984 Nov. 64(5):672-4. [Medline].
Cunanan RG, Courey NG, Lippes J. Laparoscopic findings in patients with pelvic pain. Am J Obstet Gynecol. 1983 Jul 1. 146(5):589-91. [Medline].
Hughes E, Brown J, Collins JJ, Farquhar C, Fedorkow DM, Vandekerckhove P. Ovulation suppression for endometriosis. Cochrane Database Syst Rev. 2007 Jul 18. CD000155. [Medline].
Vercellini P, Crosignani PG, Abbiati A, Somigliana E, Viganò P, Fedele L. The effect of surgery for symptomatic endometriosis: the other side of the story. Hum Reprod Update. 2009 Mar-Apr. 15(2):177-88. [Medline].
Al Kadri H, Hassan S, Al-Fozan HM, Hajeer A. Hormone therapy for endometriosis and surgical menopause. Cochrane Database Syst Rev. 2009 Jan 21. CD005997. [Medline].
Alborzi S, Momtahan M, Parsanezhad ME, et al. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004 Dec. 82(6):1633-7. [Medline].
Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008 Apr 16. CD004992. [Medline].
Waller KG, Shaw RW. Gonadotropin-releasing hormone analogues for the treatment of endometriosis: long-term follow-up. Fertil Steril. 1993 Mar. 59(3):511-5. [Medline].
Weissman AM, Hartz AJ, Hansen MD, Johnson SR. The natural history of primary dysmenorrhoea: a longitudinal study. BJOG. 2004 Apr. 111(4):345-52. [Medline].
Proctor ML, Smith CA, Farquhar CM, Stones RW. Transcutaneous electrical nerve stimulation and acupuncture for primary dysmenorrhoea. Cochrane Database Syst Rev. 2002. CD002123. [Medline].
Johnson NP, Farquhar CM, Crossley S, et al. A double-blind randomised controlled trial of laparoscopic uterine nerve ablation for women with chronic pelvic pain. BJOG. 2004 Sep. 111(9):950-9. [Medline].
Zullo F, Palomba S, Zupi E, et al. Long-term effectiveness of presacral neurectomy for the treatment of severe dysmenorrhea due to endometriosis. J Am Assoc Gynecol Laparosc. 2004 Feb. 11(1):23-8. [Medline].
Proctor ML, Latthe PM, Farquhar CM, Khan KS, Johnson NP. Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev. 2005 Oct 19. CD001896. [Medline].
Panganamamula UR, Harmanli OH, Isik-Akbay EF, et al. Is prior uterine surgery a risk factor for adenomyosis?. Obstet Gynecol. 2004 Nov. 104(5 Pt 1):1034-8. [Medline].
Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Surv. 1993 Jun. 48(6):357-87. [Medline].
ACOG. ACOG technical bulletin. Chronic pelvic pain. Number 223--May 1996 (replaces no. 129, June 1989). American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet. 1996 Jul. 54(1):59-68. [Medline].
Demco L. Pain mapping of adhesions. J Am Assoc Gynecol Laparosc. 2004 May. 11(2):181-3. [Medline].
Chan CL, Wood C. Pelvic adhesiolysis--the assessment of symptom relief by 100 patients. Aust N Z J Obstet Gynaecol. 1985 Nov. 25(4):295-8. [Medline].
Peters AA, Trimbos-Kemper GC, Admiraal C, et al. A randomized clinical trial on the benefit of adhesiolysis in patients with intraperitoneal adhesions and chronic pelvic pain. Br J Obstet Gynaecol. 1992 Jan. 99(1):59-62. [Medline].
Bost BW. Deflecting sigmoid adhesions: an anatomic cause of chronic pelvic pain and irritable bowel syndrome. Obstet Gynecol. 2001 Apr. 97(4 Suppl 1):S27.
Keltz MD, Gera PS, Olive DL. Prospective randomized trial of right-sided paracolic adhesiolysis for chronic pelvic pain. JSLS. 2006 Oct-Dec. 10(4):443-6. [Medline].
Ahmad G, Duffy JM, Farquhar C, Vail A, Vandekerckhove P, Watson A, et al. Barrier agents for adhesion prevention after gynaecological surgery. Cochrane Database Syst Rev. 2008 Apr 16. CD000475. [Medline].
Roberts LM, Sanfilippo JS, Raab S. Effects of laparoscopic lavage on adhesion formation and peritoneum in an animal model of pelvic inflammatory disease. J Am Assoc Gynecol Laparosc. 2002 Nov. 9(4):503-7. [Medline].
Drossman DA. Chronic functional abdominal pain. Am J Gastroenterol. 1996 Nov. 91(11):2270-81. [Medline].
Peters KM, Carrico DJ, Kalinowski SE, Ibrahim IA, Diokno AC. Prevalence of pelvic floor dysfunction in patients with interstitial cystitis. Urology. 2007 Jul. 70(1):16-8. [Medline].
Slocumb JC. Chronic somatic, myofascial, and neurogenic abdominal pelvic pain. Clin Obstet Gynecol. 1990 Mar. 33(1):145-53. [Medline].
Langford CF, Udvari Nagy S, Ghoniem GM. Levator ani trigger point injections: An underutilized treatment for chronic pelvic pain. Neurourol Urodyn. 2007. 26(1):59-62. [Medline].
Abbott JA, Jarvis SK, Lyons SD, Thomson A, Vancaille TG. Botulinum toxin type A for chronic pain and pelvic floor spasm in women: a randomized controlled trial. Obstet Gynecol. 2006 Oct. 108(4):915-23. [Medline].
Weiss JM. Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency-frequency syndrome. J Urol. 2001 Dec. 166(6):2226-31. [Medline].
Clemons JL, Arya LA, Myers DL. Diagnosing interstitial cystitis in women with chronic pelvic pain. Obstet Gynecol. 2002 Aug. 100(2):337-41. [Medline].
FitzGerald MP, Brensinger C, Brubaker L, Propert K,. What is the pain of interstitial cystitis like?. Int Urogynecol J Pelvic Floor Dysfunct. 2006 Jan. 17(1):69-72. [Medline].
Hanno PM, Sant GR. Clinical highlights of the National Institute of Diabetes and Digestive and Kidney Diseases/Interstitial Cystitis Association scientific conference on interstitial cystitis. Urology. 2001 Jun. 57(6 Suppl 1):2-6. [Medline].
van Ophoven A, Pokupic S, Heinecke A, Hertle L. A prospective, randomized, placebo controlled, double-blind study of amitriptyline for the treatment of interstitial cystitis. J Urol. 2004 Aug. 172(2):533-6. [Medline].
Soucy F, Gregoire M. Efficacy of prednisone for severe refractory ulcerative interstitial cystitis. J Urol. 2005 Mar. 173(3):841-3; discussion 843. [Medline].
Sant GR, Propert KJ, Hanno PM, et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol. 2003 Sep. 170(3):810-5. [Medline].
Parsons CL. Successful downregulation of bladder sensory nerves with combination of heparin and alkalinized lidocaine in patients with interstitial cystitis. Urology. 2005 Jan. 65(1):45-8. [Medline].
Melchior D, Packer CS, Johnson TC, Kaefer M. Dimethyl sulfoxide: does it change the functional properties of the bladder wall?. J Urol. 2003 Jul. 170(1):253-8. [Medline].
Mayer R, Propert KJ, Peters KM, et al. A randomized controlled trial of intravesical bacillus calmette-guerin for treatment refractory interstitial cystitis. J Urol. 2005 Apr. 173(4):1186-91. [Medline].
Dawson TE, Jamison J. Intravesical treatments for painful bladder syndrome/ interstitial cystitis. Cochrane Database Syst Rev. 2007 Oct 17. CD006113. [Medline].
Gittes RF. Female prostatitis. Urol Clin North Am. 2002 Aug. 29(3):613-6. [Medline].
Butrick CW. Atypical pelvic pain in gynecology. Presented at: The First National Pelvic Pain Symposium. May 12, 1995. Columbus: Ohio State University.
Kim SW, Paick JS, Ku JH. Percutaneous posterior tibial nerve stimulation in patients with chronic pelvic pain: a preliminary study. Urol Int. 2007. 78(1):58-62. [Medline].
Bornstein J, Goldstein AT, Stockdale CK,et al. 2015 ISSVD, ISSWSH, and IPPS Consensus Terminology and Classification of Persistent Vulvar Pain and Vulvodynia. J Low Genit Tract Dis. 2016 Apr. 20 (2):126-30. [Medline].
Haefner HK. Report of the International Society for the Study of Vulvovaginal Disease terminology and classification of vulvodynia. J Low Genit Tract Dis. 2007 Jan. 11 (1):48-9. [Medline].
Reed BD, Harlow SD, Sen A, Legocki LJ, Edwards RM, Arato N, et al. Prevalence and demographic characteristics of vulvodynia in a population-based sample. Am J Obstet Gynecol. 2012 Feb. 206 (2):170.e1-9. [Medline].
Goldstein A. Surgical techniques: Surgery for Vulvar Vestibulitis syndrome. J Sex Med. 2006 May. 3 (3):559-62. [Medline].
Margesson LJ. Inflammatory disorders of the vulva. Fisher BK, Margesson LJ, eds. Genital Skin Disorders Diagnosis and Treatment. St. Louis: Mosby; 1998. 155-157.
Bornstein J, Heifetz S, Kellner Y, Stolar Z, Abramovici H. Clobetasol dipropionate 0.05% versus testosterone propionate 2% topical application for severe vulvar lichen sclerosus. Am J Obstet Gynecol. 1998 Jan. 178 (1 Pt 1):80-4. [Medline].
Venkatesan, A. Paper and lecture presented at Vulvovaginal Disease Update, ISSVD. Durham, North Carolina. May 31, 2013.
Oaklander AL, Rissmiller JG. Postherpetic neuralgia after shingles: an under-recognized cause of chronic vulvar pain. Obstet Gynecol. 2002 Apr. 99 (4):625-8. [Medline].
Amarenco G, Lanoe Y, Ghnassia RT, Goudal H, Perrigot M. [Alcock's canal syndrome and perineal neuralgia]. Rev Neurol (Paris). 1988. 144 (8-9):523-6. [Medline].
Davila GW, Ghoniem GM, Kapoor DS, Contreras-Ortiz O. Pelvic floor dysfunction management practice patterns: a survey of members of the International Urogynecological Association. Int Urogynecol J Pelvic Floor Dysfunct. 2002. 13 (5):319-25. [Medline].
Margesson LJ. Contact dermatitis of the vulva. Dermatol Ther. 2004. 17 (1):20-7. [Medline].
Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut. 1999 Sep. 45 Suppl 2:II43-7. [Medline].
Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2003. CD001500. [Medline].
Bornstein J, Zarfati D, Goldshmid N, et al. Vestibulodynia--a subset of vulvar vestibulitis or a novel syndrome?. Am J Obstet Gynecol. 1997 Dec. 177(6):1439-43. [Medline].
Bourdel N, Alves J, Pickering G, Ramilo I, Roman H, Canis M. Systematic review of endometriosis pain assessment: how to choose a scale?. Hum Reprod Update. 2015 Jan. 21(1):136-152. [Medline].