bubble_chart Overview

Pelvic inflammation (pelvic inflammatory disease, PID) has two different meanings:

1. The scope of pelvic inflammation includes inflammation of the pelvic reproductive organs (uterine body, fallopian tubes, ovaries), the pelvic peritoneum, and the connective tissue surrounding the uterus (also known as the cellular tissue).
2. In some foreign literature, pelvic inflammation and salpingitis are used interchangeably, with the so-called pelvic inflammation referring specifically to salpingitis.

We agree with the first viewpoint, believing that pelvic inflammation is not limited to salpingitis.

Based on the differences in pathogens, pelvic inflammation can be further divided into two major categories: one is called "specific pelvic inflammation," which includes inflammation caused by gonococci, subcutaneous node bacilli, and childbirth-related infections (i.e., puerperium infections); the other is called "non-specific pelvic inflammation," referring to cases where the pathogens and disease causes are non-specific. This chapter mainly covers the latter, while "specific pelvic inflammation" has been detailed in another chapter.

Pelvic inflammation is a relatively common gynecological disease, particularly prevalent in countries with disordered sexual activity and rampant sexually transmitted diseases. According to U.S. statistics from 1983, approximately 850,000 women in the country suffered from pelvic inflammation that year, with about 200,000 requiring hospitalization.

In China, although sexually transmitted diseases are now less common, pelvic inflammation remains not rare due to limitations in medical conditions, insufficient attention to aseptic techniques in minor gynecological surgeries, and the widespread use of intrauterine devices. However, there are currently no large-scale statistical data on its incidence rate for reference.

bubble_chart Etiology

For many years, it has been known that gonococci, subcutaneous node bacilli, more common staphylococci, hemolytic streptococci, and large intestine bacilli are the main pathogenic bacteria causing pelvic inflammation. However, certain Chinese Taxillus Herb parasites such as filariae, schistosomes, and the mumps virus can occasionally infect the pelvic reproductive organs.

In recent years, due to improvements and advancements in smear techniques, culture methods, and serological immunology, there have been continuous new discoveries and understandings regarding the pathogens causing pelvic inflammation. Currently, it is generally believed that the pathogens of pelvic inflammation can be classified into the following major categories:

1. Endogenous sexually transmitted disease pathogens. The term "endogenous" refers to pathogens that normally Chinese Taxillus Herb in the vagina but do not cause disease. This is because the vagina contains a large number of Gram-positive, anaerobic vaginal bacilli, which produce significant amounts of lactic acid through the fermentation of glycogen in vaginal mucosal cells, maintaining the vagina in an acidic state (pH 4–5). As a result, potentially pathogenic organisms do not cause harm. However, once the environment changes (e.g., pH rises) or conditions become favorable (e.g., tissue injury), these pathogens become active and cause damage. Additionally, impaired blood supply and tissue necrosis promote the proliferation and growth of anaerobic bacteria, contributing to their pathogenic effects.

   The bacterial flora Chinese Taxillus Herb in the vagina and cervical os are often the causative agents of pelvic inflammation, including:

   Aerobic bacteria: Staphylococcus epidermidis, group B and D beta-hemolytic streptococci, fecal streptococci, large intestine bacilli, diphtheria-like bacilli, Sarcina species, and Proteus.

   Anaerobic bacteria: anaerobic lactobacilli, anaerobic streptococci, peptostreptococci, peptococci, Bacteroides fragilis, Clostridium perfringens, Eubacterium species, Veillonella, Actinomyces, Klebsiella aerogenes, and melanin-producing bacilli. Furthermore, human mycoplasma and T-strain mycoplasma are also Chinese Taxillus Herb in the normal vagina and can act as pathogens for pelvic inflammation. Some authors have even found that human mycoplasma is a relatively common pathogen causing pelvic inflammation.

2. Exogenous sexually transmitted disease pathogens

   (1) Bacteria: Common examples include gonococci and subcutaneous node bacilli, which are associated with sexual activity. Bacteria commonly found in the natural environment, such as Pseudomonas aeruginosa, are also frequent pathogens. The inflammation caused by the first two has been detailed in another chapter.

   (2) Prickly-ash-like sore (trachoma) chlamydia: In some developed and developing countries, prickly-ash-like sore (trachoma) chlamydia and gonococci are both classified as sexually transmitted diseases and are important pathogens causing pelvic inflammation. In some capitalist countries, about 50% of acute salpingitis patients have fallopian tube secretions that can culture prickly-ash-like sore (trachoma) chlamydia.

   (3) Chinese Taxillus Herb parasites: Schistosomes and filariae can also serve as infectious agents for pelvic inflammation, though such infections are rare and only occasionally seen in high-prevalence areas of these Chinese Taxillus Herb parasitic diseases.

   (4) Mumps virus: For many years, it has been known that this virus can cause oophoritis. Mumps rarely occurs in adults, and among mumps patients, only a very small percentage develop mumps virus oophoritis, with symptoms often being mild and easily overlooked. Whether other viruses can also cause pelvic inflammation remains inconclusive and requires further research.

3. Several issues regarding pathogen detection

   (1) Pathogen examination can be performed by collecting specimens through: (1) Culdocentesis to obtain pelvic fluid or pus for culture or smear examination. However, bacteria detected via puncture may be vaginal contaminants rather than true pathogens; (2) Laparoscopy or exploratory laparotomy to directly collect pus from the fimbriated end of the fallopian tube or pelvic abscess for culture or smear examination; (3) Collecting secretions from the cervical canal for culture or smear examination. If certain pathogens are identified, they may provide clues to the causative agents of pelvic inflammation; (4) For patients with severe pelvic inflammation, blood culture should be routinely performed. If bacteria are cultured, they should be considered pathogenic, as the chance of contamination is minimal.

(2) In recent years, significant improvements have been made in anaerobic bacteria detection, such as the application of gas chromatography for identifying anaerobes, which is simple and reliable. Additionally, advancements in smear staining and the use of immunofluorescence methods have greatly enhanced the accuracy of anaerobic bacteria detection. In the past, cultures of inflammatory fluids from the pelvic cavity often yielded "negative results." This could be due to two possibilities: either the bacteria in the pus were truly absent, or there were issues with the culturing techniques. Currently, it is generally recognized that Bacteroides (especially Bacteroides fragilis), Clostridium, and Peptostreptococcus are among the anaerobes responsible for severe pelvic inflammation. Therefore, continuously improving anaerobic culture techniques to increase detection rates is crucial for accurate diagnosis and effective treatment of pelvic inflammation.

(3) Pelvic inflammatory disease is often caused by mixed infections involving more than one pathogen. Even so-called specific pelvic inflammatory diseases, such as those caused by gonococci or subcutaneous node bacilli, are rarely due to a single bacterial infection and are likely to involve other pathogens, typically a mix of aerobic and anaerobic bacteria. Among the cultured bacteria, anaerobes account for approximately 60–70%. Severe pelvic inflammatory disease or cases where pelvic abscesses have formed are often mixed infections involving large intestine bacilli and certain anaerobic bacteria. The foul-smelling pus is caused by anaerobic bacteria rather than large intestine bacilli. In Sweden, it was found that 25% of patients with gonococcal salpingitis also had prickly-ash-like sore (trachoma) chlamydia cultured from their pus. Similar reports have emerged from other countries. Therefore, when treating acute pelvic inflammatory disease, the possibility of mixed infections should always be considered, and antibiotics should be used appropriately.

Pelvic abscesses present unique diagnostic and management challenges, which are discussed in a dedicated section.

Definition of abscesses: Conditions such as pyosalpinx, ovarian abscess, tubo-ovarian abscess, and abscesses resulting from acute pelvic peritonitis or acute pelvic connective tissue inflammation all fall under the category of pelvic abscesses. While these abscesses each have their own characteristics, they also share many similarities.

A wide variety of pathogens can cause pelvic inflammatory disease, and these pathogens can reach the pelvic reproductive organs or tissues through the following routes:

1. Hematogenous spread: It is well known that most cases of pelvic subcutaneous node infection involve subcutaneous node bacteria spreading from pulmonary or other organ subcutaneous node foci via the bloodstream. The rare occurrence of mumps virus-induced oophoritis is also hematogenous in origin. The deposition of schistosome eggs in the fallopian tubes is another result of hematogenous infection, and systemic bacteremia can also lead to pelvic inflammatory disease.
2. Lymphatic spread: Pelvic connective tissue inflammation, including parametritis, is often associated with cervical inflammation. Severe cervicitis, such as that caused by cervical carcinoma, frequently spreads to the pelvic connective tissue via the lymphatic system. Inflammation resulting from cervical or vaginal injury can also lead to pelvic connective tissue infection. Filariasis may occasionally cause acute pelvic lymphangitis or even inflammation of pelvic organs through lymphatic vessels, though such cases are rare.
3. Direct extension: Diffuse peritonitis, appendicitis, and acute diverticulitis can directly affect the pelvic reproductive organs. Gynecological surgeries performed via the abdominal route, especially those involving colon injury, can lead to severe pelvic infections. In cases of severe rectal infection, bacteria may occasionally penetrate the intestinal wall and directly infect pelvic organs. Even relatively simple abdominal hysterectomies can result in pelvic connective tissue inflammation at the upper vaginal stump. Vaginal hysterectomies carry an even higher risk of such complications.
4. Ascending infection: The vast majority of pelvic inflammatory diseases are caused by pathogens in the vagina ascending along the mucous membranes to infect pelvic organs. Not only gonococci ascend the mucous membranes to reach the fallopian tubes, but other pathogens do so as well. Animal experiments have confirmed that ligating the fallopian tubes prevents salpingitis. Under normal circumstances, the vagina and external cervical os harbor large numbers of pathogenic bacteria, but these do not cause disease due to the highly acidic environment. The area above the internal cervical os is sterile. The cervical canal is typically blocked by thick mucus, acting as an effective barrier to prevent vaginal bacteria from ascending into the uterine cavity and causing disease. However, if the vaginal pH changes or the cervical mucus becomes thin or disappears, vaginal bacteria can ascend into the uterine cavity. During menstruation, cervical mucus is flushed out, and menstrual blood neutralizes vaginal acidity, facilitating the activity and ascent of vaginal flora. Gonococci, which normally reside in the Bartholin's glands or cervix, often ascend along the mucous membranes after menstruation, leading to salpingitis.

In recent years, new explanations have emerged regarding the mechanism of bacterial ascent in the vagina, suggesting that it may be related to the following three factors:

(1) Sperm can serve as vectors for pathogens. In recent years, clinical practitioners in some countries have observed that some patients with pelvic inflammation are young married or unmarried women with a history of frequent sexual intercourse or promiscuity, but without sexually transmitted disease infections. Therefore, it is believed that pelvic inflammation is related to excessive sexual activity. Other researchers have identified pathogenic agents such as large intestine bacilli, gonococci, mycoplasma, toxoplasma, or cytomegalovirus on the heads of sperm through electron microscopy. When sperm pass through the cervical barrier into the uterine cavity and fallopian tubes, they carry these pathogens, leading to the occurrence of inflammation.

(II) Trichomonads as a Medium Some scholars have detected the presence of trichomonads in the uterine cavity, fallopian tube lumen, and even pelvic fluid. Electron microscopy has revealed large numbers of bacteria adhering to the surface of trichomonads, and culturing trichomonads simultaneously yields abundant Gram-negative or anaerobic bacteria. These findings have revised the old notion that trichomonad infection is merely an insignificant inflammation causing cutaneous pruritus. Instead, trichomonads are now recognized as potential carriers that can transport other pathogens upward into the uterine cavity and fallopian tubes, serving as an important medium for inflammation.

(III) Passive Transport It has been observed that charcoal particles placed in the vagina can enter the uterine cavity and even the fallopian tubes within a short time. This suggests that uterine contractions and the negative intra-abdominal pressure generated by diaphragmatic respiratory movements can draw vaginal particles into the uterine cavity. Consequently, it is theorized that pathogens present in the vagina may also be drawn into the uterine cavity by this negative pressure, leading to pelvic inflammation.

However, these new concepts regarding the pathogenesis of pelvic inflammation require further extensive research to be substantiated.

In recent years, the use of intrauterine devices (IUDs) has become one of the most important contraceptive measures. Increasing literature reports a close relationship between IUD insertion and the occurrence of pelvic inflammation. According to extensive foreign statistics, the incidence of pelvic inflammation among women using IUDs is approximately 5–10 times higher than that of the non-IUD control group, with inflammation often occurring during the initial stage of insertion. Actinomyces is a relatively common pathogenic bacterium. Women using shield-shaped or tailed IUDs exhibit a significantly higher incidence of pelvic inflammation compared to those using ring-shaped IUDs. Another noteworthy observation is that women using vaginal diaphragms or cervical caps for contraception have a lower incidence of pelvic inflammation than those using pharmaceutical contraceptives. These facts demonstrate that IUDs are indeed a significant predisposing factor for pelvic inflammation, while adding a cervical barrier (such as a cervical cap or vaginal diaphragm) during intercourse can reduce the likelihood of ascending infections.

bubble_chart Diagnosis

Precautions for diagnosing pelvic inflammation

1. When taking the medical history, attention should be paid to whether the patient uses an intrauterine device, as well as their sexual history, including frequency and promiscuity.
2. The presence of pelvic inflammation cannot be confirmed solely based on medical history, symptoms, and signs. Even if it is largely confirmed, further clarification of the nature of the inflammation is still needed.
3. Secretions obtained from the cervical os, culdocentesis, or laparoscopy should undergo bacterial smear and culture (including anaerobic culture) tests, along with drug sensitivity tests, to more accurately identify the pathogenic microorganisms and implement targeted measures.
4. If possible, routine ultrasound examination should be performed to determine whether there are masses in the pelvic cavity. If present, their nature (whether abscesses) must be determined.

The diagnosis of a large, low-lying pelvic abscess with fluctuance upon palpation is generally straightforward. If necessary, aspiration can be performed; if pus is aspirated, the diagnosis is confirmed. If possible, the pus should undergo both aerobic and anaerobic cultures to identify the type of pathogen.

For higher-positioned parametrial inflammatory masses, gynecological examination alone is insufficient to determine whether the mass is an abscess, and culdocentesis may not be safe. Auxiliary diagnostic methods are required:

1. Ultrasound examination: For clinically suspected abscess masses, ultrasound can reveal multiple echoic areas within the mass, indicating the presence of fluid (pus). This non-invasive method is simple, convenient, and has a reliability of over 90%.
2. Radioisotope scanning: In recent years, some have used 67Ga- or 111In-labeled leukocytes for scanning to diagnose abdominal abscesses, achieving high accuracy. The accuracy of 111In scanning can reach 85–100%. However, this method is not yet widely used clinically.
3. Computed tomography (CT): This method can achieve 100% accuracy in diagnosing abdominal abscesses. However, due to its high cost, it is not yet widely applicable.

bubble_chart Treatment Measures

Principles of Treatment

1. For patients with acute pelvic inflammation, active and thorough treatment should be administered to prevent the inflammation from becoming chronic, as the latter is more stubborn and may affect reproductive function.
2. Targeted treatment against pathogens. Pelvic inflammation is often a mixed infection. If bacterial culture is positive, the most effective antibiotics can be selected based on drug sensitivity tests. If culture conditions are unavailable or anaerobic bacteria cannot be cultured, antibiotics effective against such bacteria should be chosen under the assumption of their presence. In recent years, metronidazole has been widely used to treat anaerobic infections due to its strong bactericidal effect, minimal side effects, and low cost.
3. For patients with inflammatory masses, surgical intervention should be considered if antibiotic treatment proves ineffective.

Pelvic Abscess

1. Antibiotic Treatment: Historically, the primary treatment for pelvic abscesses relied on incision and drainage or abscess removal. With the emergence of broad-spectrum antibiotics, antibiotic therapy has become another effective measure for preventing and treating certain pelvic abscesses.

   The selected drugs should be effective against anaerobic bacteria (especially Bacteroides fragilis) and preferably broad-spectrum. Currently, clindamycin, metronidazole, and third-generation cephalosporins such as cefoxitin are commonly used to treat pelvic abscesses (dosage as mentioned earlier). Anaerobic bacteria cause significant tissue damage, impairing local blood circulation and making it difficult for drugs to reach the infected area. However, it has been found that clindamycin can achieve high concentrations in abscesses due to its transport by polymorphonuclear leukocytes, thereby enhancing its efficacy.

   Drug therapy is generally limited to treating early-stage tubo-ovarian abscesses. Effective treatment is defined as the disappearance or alleviation of symptoms, normalization of body temperature, reduction in mass size, and minimal tenderness. Reported efficacy rates for drug therapy reach approximately 70%. However, whether drug treatment alone can achieve a complete cure—i.e., total resolution of the mass and no recurrence of the abscess—remains uncertain. If drug therapy leaves a large residual mass, surgical removal is often necessary. During drug treatment, vigilance for potential abscess rupture is essential. If spontaneous rupture occurs suddenly, releasing pus into the abdominal cavity, it can be life-threatening, necessitating immediate surgical intervention.

2. Surgical Treatment

   (1) Incision and Drainage: For abscesses located near the pelvic floor, posterior colpotomy and drainage are often employed. After significant pus drainage, symptoms can rapidly improve. Some advocate placing a thick rubber tube during posterior colpotomy, with the upper end reaching the abscess cavity and the lower end remaining in the vagina. However, if the incision is large and drainage is adequate, a rubber tube may not be necessary. Others suggest using a syringe to inject antibiotics into the abscess cavity, with repeated aspiration and injection serving as an alternative drainage method. Oral or intramuscular antibiotics can be administered concurrently with drainage.

This method is particularly effective for abscesses caused by acute pelvic cellulitis, especially those following hysterectomy. Once all pus is drained, the patient can achieve a cure. For intraperitoneal abscesses, drainage may only provide temporary symptom relief, and subsequent laparotomy for lesion removal is often required once the acute inflammatory phase has subsided, making the procedure safer and more feasible.

(2) Surgical Excision of Abscess: Many believe that, except for pelvic abscesses easily drained via the vagina, surgical removal is the fastest and most effective treatment for other intraperitoneal abscesses, including pyosalpinx, ovarian abscess, and tubo-ovarian abscess. Surgery can be performed after 48–72 hours of antibiotic treatment following hospital admission.

The extent of surgery should be determined based on the patient's condition. For young patients who have no children, only the affected side's uterine adnexa should be removed. If the contralateral adnexa appears normal, it should be preserved to allow the patient the opportunity for fertility. If the patient already has children and is older, bilateral adnexa and total hysterectomy should be performed to prevent recurrence. If severe damage to bilateral adnexa is found during surgery, bilateral adnexa and total hysterectomy should be performed regardless of the patient's age. Younger patients can be treated with estrogen postoperatively to alleviate the symptoms of artificial amenorrhea.

By adopting this method, not only can therapeutic effects be quickly achieved, but serious consequences caused by abscess rupture can also be avoided. However, even if antibiotic treatment is administered for 2-3 days before surgery, gentle manipulation should still be exercised during the operation to avoid injuring the intestines or causing a large amount of pus to spill into the abdominal cavity.