Pelvic Pain

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Chapter 21 Pelvic Pain

Pelvic pain is a frequent complaint in gynecology. It may be cyclic and associated with menstruation, sudden in onset (acute), or chronic, lasting for more than 6 months. Half of all menstruating women are affected by painful menstruation or dysmenorrhea, making it the most common type of pelvic pain. Ten percent of these women have severe symptoms necessitating time off from work or school.

Dysmenorrhea

Dysmenorrhea may be primary, when there is no readily identifiable cause, or secondary to organic pelvic disease. The typical age range of occurrence for primary dysmenorrhea is between 17 and 22 years, whereas secondary dysmenorrhea is more common in older women.

PRIMARY DYSMENORRHEA

Pathophysiology

Primary dysmenorrhea occurs during ovulatory cycles and usually appears within 6 to 12 months of the menarche. The etiology of primary dysmenorrhea has been attributed to uterine contractions with ischemia and production of prostaglandins. Women with dysmenorrhea have increased uterine activity, which results in increased resting tone, increased contractility, and increased frequency of contractions. During menstruation, prostaglandins are released as a consequence of endometrial cell lysis, with instability of lysosomes and release of enzymes that break down cell membranes.

The evidence that prostaglandins are involved in primary dysmenorrhea is convincing. Menstrual fluid from women with this disorder have higher than normal levels of prostaglandins (especially prostaglandin F_2α [PGF_2α] and PGE₂), and these levels can be reduced to below normal with nonsteroidal antiinflammatory drugs (NSAIDs), which are effective treatments. Infusions of PGF_2α or PGE₂ reproduce the discomfort and many of the associated symptoms such as nausea, vomiting, and headache. Secretory endometrium contains much more prostaglandin than proliferative endometrium. Women with primary dysmenorrhea have upregulated cyclooxygenase (COX) enzyme activity as a major cause of their pain. Anovulatory endometrium (without progesterone) contains little prostaglandin, and these menses are usually painless.

Figure 21-1 summarizes the relationships among endometrial cell wall breakdown, prostaglandin synthesis, uterine contractions, ischemia, and pain.

FIGURE 21-1 Postulated mechanism of pain generation in primary dysmenorrhea. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenase, the enzyme that catalyzes the formation of prostaglandins from arachidonic acid. Hormonal contraceptives that block ovulation significantly reduce the formation of prostaglandins. Both drugs mitigate this mechanism of pain and are effective treatment for primary dysmenorrhea.

(Modified from Dawood MY: Hormones, prostaglandins and dysmenorrhea. In Dawood MY [ed]: Dysmenorrhea. Baltimore, Williams & Wilkins, 1981.)

The clinical features of primary dysmenorrhea are summarized in Box 21-1. Cramping usually begins a few hours before the onset of bleeding and may persist for hours or days. It is localized to the lower abdomen and may radiate to the thighs and lower back. The pain may be associated with altered bowel habits, nausea, fatigue, dizziness, and headache.

Treatment

Box 21-2 lists the treatment options for primary dysmenorrhea. NSAIDs, which act as COX inhibitors, are highly effective in the treatment of primary dysmenorrhea. Typical examples include ibuprofen (400 mg every 6 hours), naproxen sodium (250 mg every 6 hours), and mefenamic acid (500 mg every 8 hours). Decreasing prostaglandin production by enzyme inhibition is the basis of all NSAIDs. Hormonal contraceptives such as oral contraceptive pills (OCs), patches, or transvaginal rings reduce menstrual flow and inhibit ovulation and are also effective therapy for primary dysmenorrhea. Extended cycle use of OCs or the use of long-acting injectable or implantable hormonal contraceptives or progestin-containing intrauterine devices minimizes the number of withdrawal bleeding episodes that users have. Some patients may benefit from using both hormonal contraception and NSAIDs.

Resistant cases may respond to tocolytic agents (e.g., salbutamol), a calcium blocker (e.g., nifedipine), or high-dose continuous daily progestogens (especially medroxyprogesterone acetate or dydrogesterone). Nonpharmacologic pain management, particularly acupuncture or transcutaneous electrical stimulation, may be useful, as are psychotherapy, hypnotherapy, and heat patches. Surgical procedures such as presacral neurectomy and uterosacral ligament section have been largely abandoned.

If a patient fails to respond to hormonal contraception and NSAID therapy, the diagnosis of primary dysmenorrhea should be questioned and consideration given to a secondary cause. Ultrasonic imaging, laparoscopy, and hysteroscopy with directed biopsy should be performed to exclude pelvic disease.

SECONDARY DYSMENORRHEA

Pathophysiology

The mechanism of pain in secondary dysmenorrhea depends on the underlying (secondary) cause and in most cases is not well understood. Prostaglandins may also be involved in this type of dysmenorrhea, although NSAIDs and hormonal contraceptives that do not suppress menses altogether are less likely to provide satisfactory pain relief.

Clinical Features

The clinical features of some of the underlying causes of secondary dysmenorrhea are summarized in Box 21-3. In general, secondary dysmenorrhea is not limited to the menses and can occur before as well as after the menses. In addition, secondary dysmenorrhea is less related to the first day of flow, develops in older women (in their 30s or 40s), and is usually associated with other symptoms such as dyspareunia, infertility, or abnormal uterine bleeding.

BOX 21-3 Characteristics of Some Causes of Secondary Dysmenorrhea

Endometriosis

Pain extends to premenstrual or postmenstrual phase or may be continuous; may also have deep dyspareunia, premenstrual spotting, and tender pelvic nodules (especially on the uterosacral ligaments); onset is usually in the 20s and 30s but may start in teens.

Pelvic Inflammation

Initially pain may be menstrual, but often with each cycle it extends into the premenstrual phase; may have intermenstrual bleeding, dyspareunia, and pelvic tenderness.

Adenomyosis, Fibroid Tumors

Uterus is generally clinically and symmetrically enlarged and may be mildly tender; dysmenorrhea is associated with a dull pelvic dragging sensation.

Ovarian Cysts (Especially Endometriosis and Luteal Cysts)

Should be clinically evident

Pelvic Congestion

A dull, ill-defined pelvic ache, usually worse premenstrually, relieved by menses; often a history of sexual problems

Treatment

Management consists of the treatment of the underlying disease. The treatments used for primary dysmenorrhea (Box 21-2) are often helpful. Other specific treatments are discussed in the chapters dealing with the underlying causes.

Acute Pelvic Pain

Acute pain is sudden in onset and is usually associated with significant neuroautonomic reflexes such as nausea and vomiting, diaphoresis, and apprehension. It is important for the gynecologist to be aware of both the gynecologic and nongynecologic causes of acute pelvic pain (Box 21-4). Delay of diagnosis and treatment of acute pelvic pain increase the morbidity and even mortality.

Adnexal accidents, including torsion or rupture of an ovarian (Figure 21-2) or fallopian tube cyst, can cause severe lower abdominal pain. Normal ovaries and fallopian tubes rarely undergo torsion, but cystic or inflammatory enlargement predisposes to these adnexal accidents. The pain of adnexal torsion can be intermittent or constant, is often associated with nausea, and has been described as reverse renal colic because it originates in the pelvis and radiates to the loin. An enlarging pelvic mass is found on examination and ultrasound with decreased or absent blood flow to the adnexa on Doppler ultrasound studies. The need for surgical intervention is common and urgent.