Pelvic pain of acute onset may result from pelvic inflammatory disease (PID), ectopic pregnancy, torsion of the fallopian tube or ovary, rupture of an ovarian cyst, extrapelvic pathology such as acute appendicitis, or ureteral stones.

Torsion of the fallopian tube with or without ovarian involvement is seen most commonly in women of reproductive age. The adnexa may be normal except for the resulting ischemia, although ovarian cysts are seen in most cases. Severe, acute, unilateral pain and distension are found without an elevation of white blood cell count, fever, or increased sedimentation rate, unless complicated by ischemic necrosis. Most patients have an adnexal mass on ultrasound, and Doppler exam shows absent ovarian blood flow.

Ovarian cysts may spontaneously rupture or twist on their pedicles. Rupture can be associated with rapid blood loss, similar to a ruptured ectopic pregnancy. More commonly, only small amounts of fluid or blood are leaked, resulting in unilateral and often recurrent discomfort. Torsion of the pedicle of the cyst can cause ischemia and lead to extreme pain with acute peritoneal signs, fever, and leukocytosis.

Extrapelvic pathology that can cause acute pelvic pain includes appendicitis, kidney stones, urinary tract infections, bleeding from a Meckel diverticulum, intestinal obstructions, intestinal abscesses, or even an occult pelvic insufficiency fracture in an older woman.

Conditions that result in recurrent or chronic pelvic pain are generally less urgent than those responsible for acute pain, but they can be problematic for patients and among the most difficult to diagnose for clinicians. Common etiologies include primary dysmenorrhea; secondary dysmenorrhea caused by endometriosis, adenomyosis, and IUDs; chronic PID; uterine fibroids; ovarian cysts; nongynecologic pathology such as adhesions, inflammatory bowel disease, or irritable bowel syndrome; and psychogenic pain. Attention to the details of the clinical presentation often yields important diagnostic clues.

Dysmenorrhea represents the major source of recurrent pelvic pain. It is classified as primary when there is no pelvic pathology and secondary when it occurs in the setting of an underlying gynecologic problem, such as endometriosis, PID, or IUD use. Primary dysmenorrhea affects as many as 50% of postpubertal women. It occurs in ovulatory cycles and therefore begins within a few years of menarche when the cycles become regular.
The pain occurs at the onset of menstrual blood flow and generally lasts for 48 to 72 hours. It is cramping in nature and can be located in the suprapubic region, the low back, or the inner aspect of the thighs. Dysmenorrhea that begins years after the onset of regular cycles is usually secondary to gynecologic pathology.

Menstrual pain occurs because of increased prostaglandin (PG) production and release by the endometrium, which leads to abnormal uterine muscle activity. Several studies showed increased menstrual fluid PG levels (primarily PGF_2a) and increased circulating leukotriene and vasopressin levels in women with primary dysmenorrhea. High levels of these hormones lead to increased uterine tone and dysrhythmic contractions followed by reduction in uterine blood flow and ischemia. The pain may be from the abnormal contractions, uterine ischemia, or stimulation of sensory pain fibers by the PGs and bradykinin. Nonsteroidal antiinflammatory drugs (NSAIDs), which reduce PG synthesis, are extremely effective at reducing menstrual pain.

Many physiologic changes occur during the menstrual cycle. Up to 30% of women suffer from premenstrual syndrome (PMS) and appear to have an abnormal response to the normal hormonal changes associated with the menstrual cycle, particularly those in the luteal phase. The most severe form of PMS has been termed premenstrual dysphoric disorder (PMDD), which affects 3% to 8% of reproductive-age women and is defined by significant impairment of function. The precise mechanisms by which normal hormonal changes result in symptoms are poorly understood, but their effects on serotonergic and γ-aminobutyric acid receptors appear to be important. For example, serotonergic activity decreases in some women with PMS during the luteal phase. Personality testing done during symptomatic periods reveals abnormalities, but retesting at other stages of the menstrual cycle shows resolution of the changes, suggesting that psychological factors may be a manifestation rather than a cause of the problem. PMS is believed to be pathophysiologically distinct from dysmenorrhea, unrelated to PGs, and unresponsive to nonsteroidals. It does respond rapidly to selective serotonin reuptake inhibitors (SSRIs), even when intermittently dosed during the luteal phase, supporting the importance of serotonin in the pathophysiology and a distinction from routine depression.

Symptoms, which may seriously disrupt daily activities and impair lifestyle (and must do so for PMDD to be diagnosed), include physical symptoms such as fatigue, headache, joint or muscle pain, bloating, headache, breast tenderness, or weight gain, along with psychological symptoms including irritability, food cravings, inability to concentrate, anxiety, and depression. Onset is typically 7 to 10 days before menses commence, continues through 4 days of blood flow, and is recurrent with each cycle. The diagnosis of PMS and PMDD is based on the history of symptoms and their correlation with the menstrual cycle. It is helpful to have patients keep a prospective daily chart of their symptoms and their menses for two or more months to assess the pattern.

Endometriosis is presumed to be a common cause of secondary dysmenorrhea, although it may also be asymptomatic. Endometriosis is caused by the presence of functioning ectopic endometrial tissue, located in such places as the ovaries, uterosacral ligaments, cul-de-sac, and peritoneum. It occurs in 6% to 10% of reproductive women and in up to 50% of women with infertility. In symptomatic women, pain can be continuous or intermittent, and is frequently associated with dysmenorrhea starting days before the menstrual cycle. It is usually bilateral and may radiate to the rectum or perineal region. There is frequently a history of infertility, dyspareunia, or menorrhagia. Symptoms of endometriosis depend on actively functioning endometrial tissue, with resolution at menopause. The frequency of dysmenorrhea has been found to be no different in patients with endometriosis than with normal control subjects; however, patients with extensive endometriosis (stage III or IV by laparoscopy) were more likely to have acyclic pain. Otherwise, stage of endometriosis does not affect the severity or presence of symptoms, supporting the theory that a chronic inflammatory response is responsible for the symptoms. Diagnosis of endometriosis can only be made by direct visualization of implants on laparoscopy or laparotomy, although physical findings that may suggest the disorder include focal pain or tenderness on pelvic exam, a pelvic mass, immobile pelvic organs, and rectovaginal nodules.

Adenomyosis, also referred to as “uterine fibroids,” is caused by the presence of functioning ectopic endometrial tissue in the myometrium. It appears to be most common in women aged 41 to 50 years, although this may be a reflection of historic diagnosis based on hysterectomy, whereas it is now suggested by pelvic magnetic resonance imaging (MRI) in younger woman. The condition can cause menorrhagia, dysmenorrhea, and an enlarged, often tender uterus, although one third of women are asymptomatic. Pain may be referred to the back and rectum.

As noted, PID may also cause chronic pelvic pain, either because of untreated infection or as a complication of previous infection. It is a common cause of chronic pelvic pain in populations with a high prevalence of sexually transmitted disease. A history of previous sexually transmitted disease, dyspareunia, menstrual irregularity, backache, rectal pressure, or pelvic pain with fever is often obtained. The physical examination may reveal tender, thickened adnexa in those with active infection.