Diagnostic laparoscopy is reserved for establishing the diagnosis in patients who have acute abdomen of uncertain cause, for elucidating the nature of an ambiguous adnexal mass, or for delineating whether a pregnancy is intrauterine or extrauterine (if ultrasound results and βhCG are equivocal). Visualization is hampered if diagnostic laparoscopy is performed for a large pelvic mass (>12 cm) and is relatively contraindicated in patients with peritonitis, severe ileus, or bowel obstruction. In these settings, laparotomy is preferable. The majority of patients with pelvic pain and a normal pelvic ultrasound have improvement or resolution of symptoms with conservative therapy and do not require surgical intervention (33).
Cyclic Pain: Primary and Secondary Dysmenorrhea
Dysmenorrhea is a common gynecologic disorder affecting as many as 60% of menstruating women (34). Primary dysmenorrhea refers to menstrual pain without pelvic pathology, whereas secondary dysmenorrhea is defined as painful menses associated with underlying pathology. Primary dysmenorrhea usually appears within 1 to 2 years of menarche, when ovulatory cycles are established. The disorder affects younger women but may persist into their 40s. Secondary dysmenorrhea usually develops years after menarche and can occur with anovulatory cycles. The differential diagnosis of secondary dysmenorrhea is outlined in Table 16.3 (2).
Primary Dysmenorrhea The etiology of primary dysmenorrhea includes excessive or imbalanced amount of prostanoids secreted from the endometrium during menstruation. The prostanoids result in increased uterine contractions with a dysrhythmic pattern, increased basal tone and increased active pressure. Uterine hypercontractility, decreased uterine blood ﬂow, and increased peripheral nerve hypersensitivity contribute to pain (35,36). Prostaglandin compounds are found in higher concentrations in secretory endometrium than in proliferative endometrium. The decline of progesterone levels in the late luteal phase triggers lytic enzymatic action, resulting in a release of phospholipids with the generation of arachidonic acid and activation of the cyclo-oxygenase (COX) pathway. The biosynthesis and metabolism of prostaglandins and thromboxane derived from arachidonic acid are depicted in Figure 16.1. Increased synthesis of prostanoids in women with primary dysmenorrhea results in higher uterine tone with high-amplitude contractions causing dysmenorrhea (36). It is theorized that women suffering from dysmenorrhea have up-regulated COX enzyme activity and prostanoid synthase activity. This led to the use of nonsteroidal anti-inﬂammatory drugs (NSAIDs), which act as COX enzyme inhibitors, for therapy (37).
The pain of primary dysmenorrhea usually begins a few hours before or just after the onset of a menstrual period and may last 48 to 72 hours. The pain is similar to labor, with suprapubic cramping, and may be accompanied by lumbosacral backache, pain radiating down the anterior thigh, nausea, vomiting, diarrhea, and rarely syncopal episodes. The pain of dysmenorrhea is colicky in nature and, unlike abdominal pain that is caused by chemical or infectious peritonitis, is relieved by abdominal massage, counter-pressure, or movement of the body.
On examination, the vital signs are normal. The suprapubic region may be tender to palpation. Bowel sounds are normal, and there is no upper abdominal tenderness and no abdominal rebound tenderness. Bimanual examination at the time of the dysmenorrheic episode often reveals uterine tenderness; severe pain does not occur with movement of the cervix or palpation of the adnexal structures. The pelvic organs are normal in primary dysmenorrhea.