Acute pain is intense and characterized by sudden onset, sharp rise, and short course. Cyclic pain refers to pain that occurs with a definite association to the menstrual period. Dysmenorrhea, or painful menstruation, is the most common cyclic pain phenomenon and is classified as primary or secondary on the basis of associated anatomic pathology (1). Chronic pelvic pain is defined as pain of greater than 6 months in duration, localized to the anatomic pelvis, and severe enough to cause functional disability or necessitating medical care (2).
Whereas acute pain is generally associated with autonomic reﬂex responses, such as nausea, emesis, diaphoresis, and apprehension, such autonomic reﬂex responses are not present in women with chronic pelvic pain. Acute pain is affiliated with signs of inﬂammation or infection, such as fever and leukocytosis, which are absent in chronic pain states. The pathophysiology of acute pelvic pain involves mediators of inﬂammation present in high concentration as a result of infection, ischemia, or chemical irritation.
By contrast, the etiology of chronic pelvic pain often involves changes in modulation or “upregulation” of normally nonpainful stimuli. Pain is out of proportion to the degree of tissue damage (3). Chronic pain is thus characterized by physiologic, affective, and behavioral responses that differ from those associated with acute pain (4). An inﬂammatory lesion, such as endometriosis, for example, can set up an environment of chronic neurogenic inﬂammation or stimulation, which can result in “plastic” changes in the peripheral and central nervous system and the persistence of chronic pain (5–7). Moreover, genetic predisposition, adverse environmental pressures, and hormonal milieu are thought to increase the vulnerability and predisposition for chronic pain disorders (8).
The differential diagnosis of acute pelvic pain is outlined in Table 16.1. Assessing the character of the pain helps create a differential diagnosis. Rapid onset of pain is most consistent with perforation or rupture of a hollow viscus or ischemia following the torsion of a vascular pedicle. Colic or severe cramping pain is commonly associated with muscular contraction or obstruction of a hollow viscus, such as intestine, ureter, or uterus. Pain perceived over the entire abdomen suggests a generalized reaction to an irritating ﬂuid within the peritoneal cavity such as blood, purulent ﬂuid, or contents of an ovarian cyst.
The first perception of visceral pain is a vague, deep, poorly localizable sensation associated with autonomic reﬂex responses. When the pain becomes localized to a region of the abdominal wall, the pain is called referred pain. Referred pain is well localized and more superficial and is appreciated within the nerve distribution or dermatome of the spinal cord segment innervating the involved viscus. The location of the referred pain provides insight into the location of the primary disease process (9). The innervations of the pelvic organs are outlined in Table 16.2. The upper vagina, cervix, uterus, and adnexa share the same visceral innervations with the large intestine, rectum, bladder, lower ureter, and lower small intestine. Pain from the reproductive organs, genitourinary (GU), and gastrointestinal (GI) tracts are therefore referred to the same dermatomes (10,11).
Evaluation of Acute Pelvic Pain