Free Pelvic Inflammatory Disease Report Example

Type of paper: Report

Topic: Medicine, Disease, Viruses, Vaccination, Treatment, Health, Infection, Aliens

Pages: 5

Words: 1375

Published: 2021/03/30

MED105, Medical Terminology.

Introduction. Pelvic inflammatory disease (PID) is a wide-spread infection among the women of reproductive age associated with both high (25-28%) complications rate and a severe burden to public health care (over 800 000 cases annually diagnozed in the US, with the direct treatment costs exceeding US$ 2 billion) (Agarwal, Kulshrestha & Kriplan, 2010). This paper focuses on the etiology of this disorder, its signs, symptoms, and diagnosis as well as outlines the current standards of PID management.
Etiology. PID is an umbrella term which signifies inflammation manifesting in different places of upper female genital tract (endometrium, fallopian tubes or peritoneal cavity) and caused by a wide range of pathogens. PID may present as a single agent infection or a combination of several agents (Agarwal et al., 2010; CDC, 2010). N. gonorrhoeae and C. Trachomatis as sexually transmitted organisms (STO) play a major part in PID etiology; however the role of other infectious agents such as Prevatella sp., G. vaginalis, H. influenzae, enteric Gram-negative rods (E. coli), and Streptococcus sp. have also been recognized. Cytomegalovirus (CMV), M. hominis, U. urealyticum, G.vaginalis and M. genitalium are sometimes associated with PID (CDC, 2010; Jaiyeoba, Lazenby & Soper, 2011). The rare cases of PID caused by other infectious agents such as Mycobacterium tuberculosis or Schistosoma sp. have also been described (Avan, Fatmi & Rashid, 2010). Polymicrobial flora is present in 30-50% cases and its concentration positively correlates with histological\laparoscopical findings (sites of endometrium inflammation, laparoscopically proven acute salpingitis, changed adnexal tissues) (Jaiyeoba et al., 2011).
Signs, symptoms and diagnosis. As PID is caused by wide spectrum of agents, the clinical symptoms depend on the causative pathogen, the localization and the severity of the infection. The time of symptoms manifestation can also vary depending on the infectious agent: gonococcal infection is usually characterized by a rapid onset and severe clinical symptoms such as fever (T >100.4° F, strong pelvic and\or abdominal pain), while N. gonorrhoeae and C. Trachomatis PID can go asymptomatic up to the menses, with the symptoms most frequently emerging after the menstruation (CDC, 2010). Endocervical infections are often mild, and mild PID often goes unrecognized. Due to this CDC (2010) recommends a low threshold and watchful observation of the patient’s status in case of the presence of such symptoms as lower abdominal pain (which can or can be not exacerbated by exercise, coitus, change of body position), constant or intermittent pelvic pain accompanied by nausea and vomiting, abnormal bleeding, dyspareunia, abnormal vaginal discharge\ urinary frequency etc. For the reason of clinical manifestations and duration variety, the clinical diagnosis of PID is imprecise (CDC, 2010). The differential diagnosis should be made with ectopic pregnancy, endometriosis, cervicitis, appendicitis, upper and lower urinary tract infections (cystitis, pyelonephritis). PID can be suspected in young sexually active women of reproductive age with pelvic pain, accompanied or not accompanied by other above mentioned symptoms. However all of these symptoms are non-specific for PID. Lower abdominal pain can be caused by ectopic pregnancy or acute appendicitis, and the positive predictive value (PPV) of a clinical diagnosis of acute PID may vary significantly. CDC (2010) set a list of criteria for PID diagnosis in the young sexually active women with abdominal pain. If any other disease than PID is excluded in course of differential diagnosis, the treatment for PID is started in case of the presence of pelvic\lower abdominal pain and cervical motion and\or uterine and\or adnexal tenderness at pelvic examination (CDC,2010). Urethral sampling can be obtained if gonococcal\chlamydial origin of the disease is suspected. Vaginal microscopy reveals purulent discharge, the presence of trichomonads or cervical infection with N. gonorrhoeae or C. trachomatis, as well as abnormally elevated levels of leukocytes. High levels of C-reactive protein and\ or erythrocyte sedimentation rate can be observed as a result of acute inflammation (Jaiyeoba et al., 2011). PID cannot be confirmed by any single test as there is no test highly specific for it, but cumulative laboratory tests results can corroborate the clinical findings (CDC, 2010). Imaging studies (pelvic ultrasonography or computer tomography) can be helpful to exclude appendicitis or symptomatic ovarian cysts (Jaiyeoba et al., 2011) and MRI \doppler can visualize such signs of PID as thickened, fluid-filled tubes with or without free pelvic fluid or tubal hyperemia (CDC,2010). Finally the clinicians should be aware that endometritis can present as the only PID symptom in some cases where invasive procedures such as endometrial biopsy or even laparoscopy may be necessary (CDC, 2010).
Predisposing/risk factors. Multiple sexual partners, prior STOs experience, a history of sexual abuse are named among most common risk factors of PID (Champion, Piper, Shain, Perdue, & Newton, 2001). HIV infection is associated with an increased risk of PID (CDC, 2010). Bacterial vaginosis is indicated as a separate risk factor by some authors, and infection with HSV-2, N. gonorrhoeae, C. trachomatis with the intercurrent bacterial vaginosis increases the risk of acute PID and acute endometritis (Cherpes et al., 2006). Young age and the abnormalities associated with it such as cervical ectopy, and invasive procedures (endometrial biopsy, curettage) are also listed among risk factors (Agarwal et al., 2011) Use of contraception ( intrauterine device) is linked to significant ( up to 9-fold) PID risk increase (CDC, 2010). Genetic factors (mediated variations in innate immune response to C. trachomatis infection) can increase susceptibility to PID (Paavanen, 2012).
Complications and prognosis. If untreated, PID can lead to infertility, recurrent infection, chronic pelvic pain, and formation of adnexal mass or ectopic pregnancies due to the tubal damage (Agarwal et al., 2011; Jaiyeoba et al., 2011). The microorganisms ascending from lower to upper genital tract enhance the inflammation, which starts as mucosal and becomes transmural. Sometimes the infection can rapidly expand over the parametrium and the bowel leading to acute peritonitis, tubo-ovarian abscess or even acute perihepatitis (Agarwal et al., 2011). The lesions and scarring in fallopian tubes as well as adhesions within the tubal lumens result in tubal infertility. The higher is the rate of PID episodes, the higher is the risk of tubal infertility in women with PID. The damage to fallopian tubes can result in the increased incidence of ectopic pregnancies. The main way to avoid the complications spreading on the endometrium and fallopian tubes or to reduce their incidence is the full elimination of the infection (CDC, 2010).
Treatment. Empirical antibiotic therapy providing coverage for wide range of pathogens is recommended by CDC (2010) for PID. The main principle is ensuring the coverage against N. gonorrhoeae and C. trachomatis, and the need of coverage against anaerobes isolated from upper reproductive tract remains unclear (CDC, 2010).Though many antimicrobial regimens exist, there is scarce evidence which of them can prevent long-term complications (Jaiyeoba et al., 2011). Treatment should be started from the point of diagnosis and in most cases is oupatient. CDC (2010) clearly outlines the cases where inpatient treatment is required (surgical emergencies, pregnancy, absence of clinical response to or intolerability of oral antimicrobial therapy (outpatient treatment), severe grade of symptoms of PID or high fever, the presence of tubo-ovarian abscess. For inpatient treatment, parenteral therapy based on intravenous (i\v) cefalosporins (cefotetan or cefoxitim 2g every 12 or 6 hours respectively combined with doxycycline 100 mg i\v or orally every 12 hours) is introduced. Ampicilline\sulbactam 3g i\v every 6 hours can be combined with doxycycline 100 mg i\v or orally every 12 hours as alternative treatment regimen (CDC, 2010).  Another alternative regimen is based on clindamycine 900mg combined with gentamicyne (2mg\kg of the weight) i\v every 8 hours .Parenteral therapy can be discontinued 24 hours after clinical improvement with the continuation of oral therapy by doxycycline. CDC recommends the combination of the latter with ceftriaxone 250 mg intramuscularly (i\m) in a single dose plus metronidazole 500 mg orally twice a day as a first-line regimen for the outpatien treatment. Oral treatment is often based on the combination of cefalosporines with metronidazole (500 mg orally twice a day 14 days) (Jaiyeoba et al., 2011) though the issues of both the optimal choice of cefalosporine and the best course duration remain unclear. Cefoxitin indicated by CDC (2014) as another alternative (2g i\m in a single dose, in combination with probenecide 1g as a single dose, and doxycycline and metronidazole) has better anaerobic coverage, but in the same time ceftriaxone provides better coverage against N. gonorrhoeae as one of the most frequent pathogens (CDC,2010). Other alternative oral regimens (amoxicillin/clavulanic acid and doxycycline or azithromycin) are either not tested enough or not tolerated well. The quinolones are not recommended any more due to increasing resistance of N. gonorrhoeae to this category of antimicrobials (CDC, 2010).
Prospective treatment. Some “gaps” in the understanding of the disease etiology as well as new emerging concepts of combination therapy give rise to new research. The evaluation of anaerobic bacteria role in acute PID requires comparing the antibiotic regimens with wide anaerobic coverage with those with little to no such coverage (CDC, 2010). Alternative regimens, such as 1 g of azithromycin in pulse dosing, can be very effective but require additional trials. Besides, placentrex injections effectiveness, in combination with antimicrobials, has also been evaluated as high, with an excellent safety profile (Dahiya &  Paul, 2013). Placentrex gives a significant clinical imrovement relieving dyspareunia, fornix tenderness and uterine restricted mobility (Aggarwal et al., 2011) and is unexpensive(Dahiya &  Paul, 2013) Still, the aim of the continuous research is finding a single wide-spectrum activity range agent which can ensure the patients’ compliance due to good safety profile, convenience of administration (once daily) and low costs (Jaiyeoba et al., 2011).,
Conclusion. PID is a disorder spread among the women of reproductive age and leading to serious complications as ectopic pregancy, tubal infertility or chronic pelvic pain. The risk factors include multiple sexual partners, young age, history of intrauterine device contraception or sexual abuse, genetic susceptibility to C. trachomatis infection, and bacterial vaginosis. There is no specific or sensitive single test for PID, and the diagnosis is made based on a set of clinical criteria and laboratory findings corroborated by imaging studies or biopsy\laparoscopy in selected cases. The clinical improvement and resolution of symptoms, with the reduction of long-term complications incidence is the main treatment goal, though there is no agreement about the antibiotic regimen ensuring the best coverage against the wide spectrum of pathogens which cause PID. Empirical therapy is based on cephalosporines accompanied by doxycycline and metronidazole, and emerging clinical evidence shows the effectiveness of new treatment schedules such as placentrex injections combined with antibiotic therapy. The optimal duration of treatment and the frequency of dosing of antimicrobial agents should be determined, and new clinical trails are required to define the best treatment regimen.


Agarwal, N., Kulshrestha, V. & Kriplan, A. (2010). Clinical eficacy of placentrex injection in pelvic inflammatory disease. J Indian Med Assoc, 108(2), 117-118, 122
Avan, B.I., Fatmi, Z., & Rashid, S. (2001). Comparison of clinical and laparascopic features of infertile women suffering from genital tuberculosis (TB) or pelvic inflammatory disease (PID) or endometriosis. J Pak Med Assoc., 51(11),393-399.
Centers for Disease Control and Prevention (CDC) (2010). Pelvic Inflammatory Disease. Retrieved from:
Champion, J.D., Piper, J., Shain, R.N., Perdue, S.T., & Newton, E.R.(2001). Minority women with sexually transmitted diseases: sexual abuse and risk for pelvic inflammatory disease. Res Nurs Health., 24(1), 38-43.
Cherpes, T.L, Wiesenfeld ,H.C, Melan, M.A, Kant, J.A, Cosentino, L.A, Meyn, L.A, Hillier, S.L.(2006). The associations between pelvic inflammatory disease, Trichomonas vaginalis infection, and positive herpes simplex virus type 2 serology. Sex Transm Dis., 33,747-752.
Dahiya, P., & Paul A. (2013). A randomised study to evaluate the efficacy and safety of placentrex injection in patients suffering from pelvic inflammatory disease. J Indian Med Assoc., 111(5), 352-353.
Jaiyeoba, O., Lazenby, G., & Soper, D.E.(2011). Recommendations and Rationale for the Treatment of Pelvic Inflammatory Disease. Expert Rev Anti Infect Ther., 9(1),61-70. 
Paavonen J. (2012). Chlamydia trachomatis infections of the female genital tract: state of the art. Ann Med., 44 (1), 18-28.

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