Pelvic Inflammatory Disease

Introduction


Pelvic inflammatory disease (PID) is a highly prevalent disorder that affects one million American women each year [1]. PID is caused by sexually transmitted infections (STIs) (see Chapter 11) which have ascended to the upper genital tract (uterus, fallopian tubes) and intraperitoneal cavity. PID is a polymicrobial infectious process; commonly isolated organisms include Chlamydia trachoma-tis, Neisseria gonorrheae, Escheria coli, and Enterococcus species. The major sequelae of this disorder include infertility, ectopic pregnancies, bowel obstructions, pelvic pain, and deep dyspareunia. This chapter reviews the relationship between PID, pelvic adhesions, and pelvic pain, and discusses how diagnosis and management can impact the long-term complications of PID.


The Link Between Pelvic Adhesions, Pelvic Pain, and Dyspareunia


Pelvic adhesions are abnormal attachments between organs and other tissues that form after any intraperitoneal insult. Adhesions form because the normal peritoneal healing process is either altered or disrupted. Adhesions form from tissue trauma that may result from infections such as PID, as well as injury, surgery, radiation, ischemia, or foreign-body reactions. Any of these triggers can then lead to activation of stromal mast cells, the first and most important trigger in the cascade of events that lead to adhesion formation.


Mast cells release vasoactive substances, such as histamine and kinins, which increase vascular permeability (see Chapter 27). In addition, mast cells induce fibrin deposition. These fibrin deposits are made up of cellular exudate, leukocytes, and macrophages. A fibrinous exudate usually forms within 3 hr of injury. The invasion of fibroblasts and blood vessels soon follows. Under normal circumstances, healing occurs by a combination of fibrosis (scarring) and mesothelial regeneration. Normally, most fibrinous exudates are transient and break down within 72 hr, but trauma-induced local suppression of peritoneal fibrinolysis predisposes to the formation of adhesions [2].


A postmortem study of motor vehicle accident victims showed that 93% of subjects who underwent prior surgery had adhesions. Only 10% of those who never had surgery had adhesions [3]. Other studies have shown that up to 20% of clinically significant pelvic adhesions are caused by inflammatory conditions, including PID. The presence of adhesions in patients who haveneverhad intra-abdominal surgery suggests that other etiologies, including PID, may be responsible. As PID is highly prevalent, it is possible that PID can be a common cause of adhesions. The American Fertility Society has developed criteria to describe the severity of adhesions [4, 5].


Significant basic science and clinical research has been directed toward the prevention of adhesions to preserve fertility. Less attention has been paid to adhesion prevention and its effects on chronic pelvic pain (CPP) or dys-pareunia. In addition, research has focused on suppressing the formation of adhesions after general and gynecologic surgery, but little effort has been spent on reducing adhesions after PID.


Studies of adhesion prevention were initiated in the 1980s and 1990s, often utilizing elaborate animal models. For example, one group of investigators found that injured rat peritoneal cells contained an increased amount of transforming growth factor beta (TGF-β) [6]. This protein was not expressed as strongly in tissues without adhesions. TGF-β has been found in human adhesions as well, suggesting that it plays a role in fibrosis and adhesion formation. If it is possible to prevent the expression of TGF-β, or suppress its action, adhesion formation may be prevented.


Although several mechanisms for this possible suppression have been suggested, one involves the omega-3 fatty acid docosahexaenoic acid (DHA). This acid is known for its ability to act as an antagonist to peroxisome proliferator activated receptors which are nuclear receptors that activate theinflammatory cascadeinvolvinglipidmetabolism, fatty acid oxidation, cytokine production, and others mediators involved in adhesion formation. When DHA is applied directly to cell cultures, it has been shown to substantially decrease levels of adhesion related markers in peritoneal adhesions and fibroblasts [7].


Landmark studies on PID were conducted in Scandinavia during the 1970s and 1980s when long-term outcomes in patients with PID were analyzed for the first time. These outcomes included pelvic pain and pelvic adhesions but neglected to study important concerns such as pelvic pain and dyspareunia. In fact, because these studies were conducted using laparoscopic evidence of PID as an inclusion criterion, many women were discovered to have Fitz–Hugh–Curtis syndrome (perihepatic adhesions), at the time of diagnosis [8]. Since that time, analyses of screening plans, antibiotic treatment regimens, outpatient versus inpatient management options, and assessments of cost-effectiveness of management have often included data on chronic pelvic pain, adhesions, quality of life, sexual function, and cost. The most notable of these studies was the large, multicenter, randomized controlled trial known as the PID Evaluation and Clinical Health (PEACH) study, in which patients with PID were followed for up to 7 years postdiagnosis. Important data regarding long-term outcomes including CPP, infertility, and quality-of-life measures were gained from these studies [9].


The U.S. Centers for Disease Control list three major criteria and five associated criteria for the diagnosis of PID (Table 20.1) [1]. Most patients with PID have fever, adnexal tenderness, and an elevated white blood cell count. However, up to two-thirds of women do not have these hallmark findings, and in many cases the PID goes unrecognized [1]. In some women, the only evidence of PID is laparoscopic findings of acute or chronic salpingitis.


Table 20.1 Centers for Disease Control criteria for PID.





























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Jun 14, 2016 | Posted by in PAIN MEDICINE | Comments Off on Pelvic Inflammatory Disease

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Minimal criteria
• Lower abdominal tenderness
• Uterine/adnexal tenderness
• Cervical motion tenderness
Additional criteria
• Oral temperature >38.3?C (101?F)
• Abnormal cervical or vaginal mucopurulent discharge
• Presence of white blood cells (WBCs) on saline microscopy of vaginal secretions
• Elevated erythrocyte sedimentation rate
• Elevated C-reactive protein level
• Laboratory documentation of cervical infection with Neisseria gonorrhoeae or Chlamydia trachomatis
Definitive criteria
• Histopathologic evidence of endometritis on endometrial biopsy Transvaginal sonography or magnetic resonance imaging techniques showing thickened, fluid-filled tubes with or without free pelvic fluid or tubo-ovarian complex