PHILIPPINE INFECTIOUS\DISEASES SOCIETY: FOR eS AND;GYNECOLOGY CLINICAL PRACTICE GUIDELINES FOR PELVIC INFLAMMATORY DISEASE De PaOverview: Epidemiology, logy, Pathogenesis, Complications Maria Lorena L. Santos, MD Clinical Diagnosis: Signs & symptoms, Risk factors, Differential diagnosis Valiant L. See, MD/Jennifer T. Co, MD/Christine D. Dizon, MD/ Mary Jane B. Noble, MD . Diagnostic Evaluation: Laboratory testing, Imaging studies, Laparoscopy, Endometrial biopsy Analyn F. Fallarme, MD/Henrietta S. Lucasan, MD/Maria Lorena L. Santos, MD Management Josefa Dawn V. Martin, MD/Sybil Lizanne R. Bravo, MD/Maria Lu D. Andal, MD PID in Special Population: Postmenopausal women, People Living with HIV/AIDS, Pregnant patients Mary Judith Q. Clemente, MD/Maria Angela R. Bandola, MD/ Lorina Q. Esteban, MD Management of Tubo-Ovarian Abscess Mary Judith Q. Clemente, MD Appendices: Algorithms Erwin R. De Mesa, MD/Raizza Lezzette P. Cruz, MD Scanned with CamScannerOVERVIEW Maria Lorena L. Santos, MD | Pelvic inflammatory disease (PID) comprises a spectrum of ‘inflammatory disorders of the upper female genital tract, including | any combination of endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis (Workowski et al., 2015). Although a definitive diagnosis of PID can be made by laparoscopic visualization of inflamed, purulent fallopian tubes, PID is generally a| clinical diagnosis and thus represents a diagnostic challenge. Diagnosis and treatment algorithms require a high index of! i suspicion for PID in any woman with pelvic or abdominal pain ;because it can cause significant reproductive health sequelae | (Mitchell et al., 2013). | References: | Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2015. MMWR | Recomm Rep 2015; 64 (3):1-140. | Mitchell C, Prabhu M. Pelvic Inflammatory Disease: Current Concepts in Pathogenesis, Diagnosis, and Treatment. Infect Dis Clin N Am 27 (2013) 793-809. 'In the Philippines, the incidence and prevalence of PID in the general population is particularly difficult to assess and current figures likely underestimate the burden of disease. All efforts at characterizing the rates of PID are complicated by several factors, including high rates of subclinical PID (Paavonen, 2005), increasing rates of outpatient diagnosis, and inaccuracies in diagnosis. | Gonococcal PID is thought to have an abrupt onset with more toxic : | Symptoms than non-gonococcal disease. Gonorrhea and Chlamydia associated infections are more likely to cause symptoms toward the | end of menses and in the first 10 days following menstruation. A review of literature and search of available published data showed |limited surveillance information in the Philippines, for the following /feasons: 1) OPD cases are not included in the POGS integrate I Statistical information system report; 2) data only include POGS-_ A Scanned with CamScanner“accredited hospitals; and 3) there is no standard nomenclature used ‘in the reporting of PID. Tables below summarize the 5-year prevalence of PID from the POGS and UP-PGH registry. | References: | Paavonen, J. Pelvic Inflammatory Disease. Journal of Me ‘Five-year National Data on Pelvic Inflammatory Disease from 89 POGS- | accredited residency training hospitals (through the Committee on Nationwide | | Statisistics) Year | Total Annual Gyne- | Pelic Inflammatory ‘Other Inflammatory Conditions cologic Admissions | Disease ‘Salpingo- | Endo- | Para- | Pelvic | Other ophontis | metrits | metiis | Absoass | PID" 2008 | 7.587 [32 4 3 i 3 16 ‘2010 | 9,322 49 5 6 | - 14 — 7 2011 | 10.714 37 6 6 1 a 14 2012 | 7.153 38 [3 15 - 7 10 2013 | 3.980 54 6 5 1 11 11 2014 | 13,374 39 13 10 : Fl : the UP-PGH | Five-year National Data on Pelvic Inflammatory Disease from t | Department of Obstetrics and Gynecology, Section of Obstetric and Gynecologic Year Number of cases [__Pelvic inflammatory Disease ‘Admissions: 7 [ 1 2010 | Ward Referrals 150 19. ‘OPD_ 208, 40 2011 | Admissions 6 7 ‘Ward Referrals 118 23 OPD 642 35, 2012 | Admissions 1 0 Ward Referrals, 121 18 mia ‘OPD 676 19 ‘Admissions 4 9 Ward Referrals 83 24 OPD 703 4 2015 [Admissions 2 0. Tig 2 ‘OPD 546 40 “data rom 2013 not avaliable Scanned with CamScanneres of PID are polymicroblal. The most common Pathogens. ae clated with PID are N. gonorrhoeae and C. trachomatis, Both are present in approximately 25%-75% of patients with PID (Eschenbach, 1975; Sweet, 2011). The relative prevalence Of these and other organisms depends on prevalence in the Population studied. The proportion of cases of PID that involve non-gonococcal, non- chlamydial etiology ranges between 9% and 23% in women with confirmed salpingitis or endometritis, even as diagnostic testing for gonorrhea and chlamydia become more sensitive. iIn these cases, the microbial community is often diverse and ‘includes anaerobes such as Peptostreptococcus Spp and Prevotella spp. Other microbes associated with PID include aerobic Gram-negative rods (e.g., E. coli), especially those / associated with bacterial vaginosis (BV), and Gram-positive organisms (streptococcus spp). Mycoplasma genitalium and 'Ureaplasma_urealyticum have also been isolated from the endometrium and fallopian tubes of women with PID. Even in women with gonorrhea or chlamydia, detection of | anaerobes in the upper Genital tract is frequent and is associated With more severe disease (Soper, 1994), euenbach DA, Buchanan TM, Pollock HM, et al, Polymicrobial etiology of acute pe arma dene N Engl J Med 1976; 288 (168-71, cases reatment of Pelvic Inflammatory: Diseases le - Infectious Dis Bhmtts 8nd Gynecology Sept 201i” Disease: A review article Biartling C, S, Persson K. M Scanned with CamScanner' There are indications that an intermittent ascent of microorganisms into the endometrial cavity and fallopian tubes may be a physiological phenomenon. The fate of such ascended organisms depends on their viability, number, pathogenicity, and local defense | | mechanisms of the host. In the case of PID, the response to the ascending organisms is an inflammatory one in the endometrium, fallopian tubes, or peritoneum. The resulting scarring of the tubes may lead to ‘infertility, ectopic pregnancy, or chronic pelvic:pain even in women | | who do not report a history of PID symptoms. : |PIDis presumed to occur in 2:stages. 1) The first stage is acquisition of a vaginal or cervical: . This infection is often sexually transmitted and may be asymptomatic. 2) The second stage is direct ascent of microorganisms from the vagina or cervix to the upper genital tract, with endometritis as an intermediate stage in the pathogenesis _of disease. Cenictis (gui) — Endometits Infection SalpingitisOophoriis/Tubo-ovarian Abscess | (Aestd rom COC PO r Module for Ctinicians, 2014) Scanned with CamScanner‘The i i Nd from the | echanisms by which microorganisms asce! d lower erie tract is unclear. Studies suggest that multiple factors, may ‘be involved. + Although cervical mucus provides a functional barrier against upward spread, the efficacy of this barrier may be decreaseg by vaginal inflammation and by hormonal changes that occur during ovulation and menstruation. Endometrial detection of gonorrhea or chlamydia is more frequent in the proliferative phase of the menstrual cycle when cervical mucus is thinner and the peristaltic contractions of the uterus move fluid cephalad. + Opening..of. the..cervix during menstruation, along with retrograde menstrual flow, may also facilitate ascent of microorganisms. * Intercourse may contribute to the ascent of infection through thythmic uterine contractions occurring during orgasm. Bacteria may also be carried along with sperm into the uterus and fallopian tubes. Inflammation may extend to un-infected parametrial structures, including the bowel. Infection may extend via spillage of purulent materials from the fallopian tubes or via lymphatic spread beyond the pelvis to produce acute peritonitis and acute perihepatitis (Fitz- | Hugh-Curtis syndrome). _Gonococcal PID is thought to have an abrupt onset with more toxic symptoms than non-gonococcal disease. Gonorrhea and Chlamydia associated infections are more likely to caus? | symptoms toward the end of menses and in the first 10 4a/° ' following menstruation. References nee 7 Kiviat NB, W.lner-Hanssen PR | Gulture-proved upper genital Surg Patho! 1990; 14: 167-75, | Paavonen J. Chlamydia trachomatis infect nt, Ant infectic i: of the ar | 2012 Feb, 44(1): 18-28 is infections of the female gonital tract: state o! | Katz OF. Human cervici Kunz G, Beil D, Deini with Eschenbach DA, et al. Endometrial histopathology in eat an tract Infection and laparoscopically diagnosed acute salping" ne 19846 ical mucus: research update. Am J Obstet Gynecol 1991; 1656 Pt 2! "aad inger H, et al. The dj yn the fem tact evidence from von ea The smamies of rap sperm transport throug | itigraPh 1 Reprod 1996;11(3):627-g2, ‘graphy of uterine peristalsis and hysterosalpingoscit 1 COC Module on Pelvic inflammatory Disease for Clinicians, 2014. Scanned with CamScanner{Complications IE SSS secede ESE SS, 'The. majority of the morbidity and public health care burden attributed to PID comes from the long-term sequelae of the i disease, including: 1) tubal factor infertility (18%) | 2) ectopic pregnancy (0.6%), and | | 8) chronic pelvic pain from adhesive disease (29%). “The adaptive immune response plays a role in the pathogenesis of | pelvic inflammatory disease because reinfection substantially jincreases the risk of tubal factor infertility (i.e., the inability to conceive because of structural or functional damage to the | ‘fallopian tubes). Infection-induced selective loss of ciliated | ‘epithelial cells along the fallopian tube epithelium can cause impaired ovum transport, resulting in tubal-factor infertility or) ectopic pregnancy. Peritoneal adhesions along the fallopian tubes may prevent pregnancy, and adhesions within the pelvis are! § related to pelvic pain. “Violin string’ adhesions between fiver and anterior abdominal wall ‘seen in Fitz-Hugh-Curtis Syndrome Adapted from: | Wiesenfeld HC, Sweet RL. Progress in the management of tuboovarian abscess. Clin Obstet Gynecol 1993:36:433-44. References | Powers K, Lazarou G, Greston WM, Mikhail M. Rupture of a tuboovarian abscess into the anterior | | abdominal wall: a case report. J Reprod Med. 2007 Mar. 52 (3):235-7. | Wiesenfeld HC, Sweet RL. Progress in the management of tuboovarian abscess. Clin Obstet | Gynecol 1993;36:433-44, Landers DV, Sweet RL. Tubo-ovarian abscess: contemporary approach to management. Rev Infect | | Dis 1983;5:676-84, Lopez-Zeno JA, Keith LG, Berger GS. The Fitz-Hugh-Curtis syndrome revisited: changing Perspectives after half a century. J Reprod Med 1985;30:567-82. Ness RB, Soper DE, Holley AL, et al. Effectiveness of inpatient and outpatient treatment strategies | for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation | ‘nd Clinical Health (PEACH) Randomized Trial. Am J Obstet Gynecol 2002; 186: 929-37. a Scanned with CamScannerDIAGNOSIS ee ae vsernater T. Co, MD Christine D. Dizon, MD/Mary Jane B. Noble, Mp STATEMENT: /Women with PID may present with subtle or nonspecific | Supporting Statement: i Depending on the severity of the infection, Patients with PID may | be minimally symptomatic or may present with toxic symptoms of: fever (temperature 38°C or higher), nausea, vomiting, and severe | pelvic and abdominal pain. Table 1: Symptoms of PID (by frequency of presentation) SYMPTOMS FREQUENCY Lower Abdominal pain 100% Abnormal vaginal discharge 55% - 75% Post-coital bleeding 40% Intermenstrual bleeding 36% Fever 30% L Urinary symptoms 19% Nausea/vomiting 10% Proctitis symptoms 7% _In a study by Freij, it showed that low abdominal pain (100%) is the most common symptom and may be present for variable Periods of time prior to diagnosis, The pain is typically described 88 dull, aching or cramps; bilateral, and constant it begins a foW ‘days after the onset of the last menstrual period and tends to b¢ accentuated by motion, exercise, or coitus. Pain from PID usually “iasts less than 7 days. If the pain lasts longer than 3 weeks, the € is present in approximately 55-75" inal bleeding, often post-coital,__ Scanned with CamScannerported in about 40% of cases. Temperature higher than 38°C | was found in 30% of cases, while nausea and vomiting (10%) | | manifest late in the clinical course of the disease. Other common | ‘symptoms include irregular vaginal bleeding (36%), urinary | ‘symptoms (19%), and proctitis symptoms (7%). The positive | predictive value of a Clinical diagnosis is 65-90% compared to | laparoscopic diagnos eferen | | Jaiyeoba O, and Soper DE. A Practical Approach to the Diagnosis of Pelvic Inflammatory Disease, | | May 2011, ' | European Guideline for the Management of Pelvic Inflammatory Disease, 2012 | Frej BJ. Acute pelvic inflammatory disease. Seminars in Adolescent Medicine, 1986 Jun;2 | 143-53. Shepherd SM. Pelvic Inflammatory Disease Clinical Presentation. Medscape. September 28, 2015 | | STATEMENT: ' | Several risk factors have been identified that increase ‘ne | likelihood of PID. Table 2: Risk factors associated with PID |. Multiple sexual partners . History of prior STIs . History of sexual abuse ._ Frequent vaginal douching _ .. Gynecologic surgical procedures such as endometrial biopsy, curettage and hysteroscopy | ._ Young age (<25 years old) - OCP use . Presence of IUD . Bilateral tubal ligation gn] | oo| ro] 2] 20] ~1] | | Supporting Statements: ‘Risk factors for PID include multiple sexual partners, a history of | prior STIs, and a history of sexual abuse. An assessment of risk for! | sexually transmitted infection (ST) may enhance the specificity of the clinical presentation of PID. Frequent vaginal douching has |been considered a risk factor, but studies reveal no clear! i ciation. Scanned with CamScanneri ical procedures such as endometrial biopsy, Cretage, and. hysteroscopy break the cervical barrier, predisposing women to ascending infections. Younger age has been found to be associated with an increased risk of PID. Likely reasons include increased cervical mucosal Permeability, a larger zone of cervical ectopy, a lower prevalence of Protective anti. chlamydial antibodies, and increased risk-taking behaviors, Studies on oral contraceptive pills (OCPs) have found differing effects on PID risks. Some authors suggest that OCPs increase the risk of endocervical infection, probably by increasing the zone of cervical ectopy. Other evidence indicates that OCPs can decrease the risk of symptomatic PID, Possibly by increasing cervical mucus viscosity, decreasing menstrual anterograde and retrograde flow, and modifying local immune responses. Other authors suggest that OCPs may not have any effect on PID incidence. The use of an intrauterine device (IUD) confers a relative risk of 0.15% for the first 3 months following insertion, but risk subsequently decreases to baseline. According to World Health Organization's (WHO) IUD clinical trial data, PID was more than six times higher during the 20 days after insertion than during later times (unadjusted rates, 9.7 versus 1.4 per 1000 woman- years, respectively). The risk was low and constant for up to eight years Of follow-up. Rates varied according to geographical area (highest in Africa and lowest in China) and were inversely associated with age. PID rates were lower among women who had IUDs inserted more recently. A retrospective chart review of patients diagnosed with PID over @ 1-year period at a large urban university hospital found 209 Patients who fulfilled the criteria for a definition of PID. Of the 209 Patients with PID, 24 ¢ and without BTL were cell count (WBC), t hospitalization, Prior Compared with respect to age, white ee emperature, admission rate, length ol ; Prior history of PID, culture results, presence | bilateral abdominal pain, Presence of rebound tenderness, 2 | complications Of tubo-ovarian abscess (TOA) and hydrosalpl" (Patients with BTL had lower WBC and were 2.5 times less likely Scanned with CamScanner 11.7%) had undergone BTL. Patients wit! |[be hospitalized compared to those patients without BTL. These | | results show that PID in the setting of a prior BTL not only exists | | put occurs with surprising frequency and deserves further study. | | Patients with BTL and PID may have a clinically milder form than | | those patients without BTL. | | | Exceptions ot the common notion that tubal occlusion protects | | from recurrent pelvic inflammatory disease (PID) do exist. Since | | 1975, 71 cases of salpingitis and 38 tubo-ovarian abscesses | | (TOA) in sterilized women have been published. The majority of | |cases of salpingitis after previous tubal occlusion (SPOT) | ‘developed more than a year after either laparoscopic or| ‘laparotomy sterilization procedures. For tubo-ovarian abscess | lafter previous tubal occlusion (TOAPOT), this time interval | ranged from several weeks to almost two decades. Most cases | of salpingitis showed inflammation of both tubal segments. |When only one segment was involved, it was generally the} | proximal segment. The appearance of the TOAPOT at the time | | of surgery was typical to TOA. The symptoms of salpingitis were | | not different from symptoms in any other case of PID, and those | |associated with TOAPOT were typical of TOA. Laboratory | ifindings included leucocytosis and growth of Neisseria | | gonorrohoea and Chlamydia trachomatis from the cervix, the | |infected tube, and the peritoneal fluid. Pus cultures obtained | | from cases of TOAPOT grew mixed or single organisms. | | Detailed histopathologic studies in tubal specimens after the, | failure of an occlusion procedure are available from cases with | |No infection. They have demonstrated distortion, loss of | Musculature, and loss of lumen configuration, all of which may have been the result of compromised blood supply to the tube. | | These findings may be extrapolated to cases of SPOT and) , TOAPOT, assuming similar changes may be present before the | | development of infection. | Scanned with CamScanner‘Tr nisms by which infection may develop in Previousiy | Secuded tubes. are divided Into three groups: The first aroun, | consists of situations where there is persistence of free Passage | between the proximal and distal portions of the tube. These |include tuboperitoneal fistula, spontaneous anastomosis at the “occlusion site, recanalization of the occluded site, incomplete, “tubal occlusion due to a faulty surgical technique or rupture of the. | weakened tubal wall, The second group consists of infections ‘initiated by the surgical procedure itself, such as introduction of: | pathogens at surgery, exacerbation of chronic PID, and | ascending infection secondary to surgical manipulation. In the. ithird group, the infection is initiated systemically by: |hematogeneous spread, lymphatic spread, or change in) | immunologic status. | References: | Shepherd SM. Pelvic Inflammatory Disease Clinical Presentation. Medscape. | | September 28, 2015 Hl Champion JD, Piper J, Shain RN, Perdue ST, Newton ER. Minority women with sexually | | transmitted diseases: sexual abuse and risk’for pelvic inflammatory disease, Ree Nure, | Health. 2001 Feb. 24(1):38-43, | Ness RB, Hillier SL, Kip KE, Richter HE, Soper DE, Stamm CA, et al. Douching, pelvic | | infammatory disease, and incident gonococcal and chlamydial genital infection in | | cohort of high-risk women. Am J Epidemiol. 2005 Jan 15. 161(2):186-95, | | Ness RB, Hillier SL, Kip KE, Soper DE, | ss Ri , E . Stamm CA, McGregor JA, et al. Bacterial | | yagigosis and risk of pelvic intammatory disease. Obstet Gynecol, 004 Oct space | 761-9. | Ness RB, Soper DE, Holley RL, Peipert J, Randall H | barrier contraception and risk of upper genital teat 4 ; Gincal Health (PEACH) study, Am J Obstet Gynecol, 2001 Jul 1ee(4) on | Farley TMM, Rowe PJ, Metrk ©, Rosenberg MJ, Chen JH. Intrauterine devices and | pelvic inflammatory disease: an international perspective Thy | | p 785-796 (28 March 1992), © Lancet, vol 339, no 8796, j | Helton JD. Risk of Cinical Pelvic Inflammatory Disease Attrib ‘ | Device. Center for Population, Health and Nutmiese ¢i cancion] intrauterine | | Development, Washington, DC 20523, USA (March 2001), mematonal | Levgur M, Duvivier R. Pelvic Inflammatory Disease afte. 7 ilizati ‘ew).| | Obstet Gynecol Surv Jan 2000, vol 58 (1). 47° \bal Sterilization (A Review). 1, Sweet RL, et al. Hormonal and isease in the PID Evaluation and | | STATEMENT: | To completely evaluate a patient with Pip, | evaluation should be done. * @ Comprehensive | Scanned with CamScannernaan Table 3: Steps in the evaluation of a woman suspected of aD 4, Abdominal examination 2, Vaginal speculum examination including inspection of the cervix for friabilty and muco-purulent cervical discharge 3. Bimanual examination, assessing for cervical motion tenderness, uterine or adnexal tenderness, and pelvic masses 4. Collection of samples of cervico-vaginal discharge (for microscopy for BVMTrichomonas and NAATS for chlamydia/gonorrhea) ic examination may reveal pelvic organ and s in the case of endometritis, while adnexal | | tenderness is elicited in salpingitis. Cervical motion tenderness i ‘another common finding in women with PID. The limitation of thi japproach is that it fails to discriminate between the differenti: | diagnoses of acute pelvic pain in reproductive-aged women. For | | this reason, the lower genital tract needs to be assessed for signs | | of inflammation. The cervical canal should be examined for the’ 'presence of yellow or green mucopus and friability. Microscopy | lof the vaginal secretions should be performed looking for! leukorrhea (more than 1 leukocyte per epithelial cell). Evaluation for bacterial vaginosis (vaginal pH, clue cells, and whiff test) and |trichomonas vaginitis is recommended. Ideally, nucleic acid) ‘amplification testing (NAAT) for Neisseria gonorrhoeae and) Chlamydia trachomatis should be performed. If the cervix is | normal and no white blood cells are noted during microscopy Of | the vaginal secretions, an alternative diagnosis should be investigated since this relial |A bimanual pelvi |uterine tendernes: bly excludes (negative predictive value | | 94.5%) upper genital tract infection. i | Reference | Mitchell C, Prabhu M. Pelvic Inflammatory Disease Current Concepts in Pathogenesis, Diagnosis and Treatment. Infect Dis Clin N Am 27 (2018) 793-809 | Statement: | ence of at. Hed clinical diagnosis of PID Is based on the pres: ast one of the minimum criteria. Scanned with CamScannerTable 4:_ Clinical and Diagnostic Criteria for PID | Additional Criteria (support a | Definitive Crea i ‘Additional Criteria (suppo! era ‘Minimum Criteria (at least 1 diagnosis of PID) (confirm the Gagnon a needed for diagnosis) PID) i : mmperature higher ‘* Histopathologic Gavel than 101-7788. °C evidence of viet taaemecs « Abnormal vaginal or endometritis SC aieeal ndatnons cervical discharge * Imaging showing | « White blood cells on saline | thickened, fluid-fileg (>10 polymorphonuclear tubes, with or: leukocytes per high-power | pelvic free uid or field tubo-ovarian complex | * Elevated erythrocyte * Doppler studies j ‘sedimentation rate (>15 ‘Suggesting pelvic | mm/h) infection Elevated C-reactive protein | « intra-abdominal Elevated white blood cell findings consistent | count > 10,000 cells/mL. with PID on | * Laboratory evidence of laparoscopy i Neisseria gonorrhoeae or | Chlamydia trachomatis | Infection je | Supporting Statements: : ; - ; | Minimum diagnostic criteria (Table 4) have been set with a high Snesites and low specificity in order to detect as many cases of a’ Gisease as possible, thus potentially avoiding the long- term reproductive sequel: : y ding 4 delayed di ; ae and economic costs associated with 'yed diagnosis and lack of treatment. The inclusion of at least | one additional criteria increases the Specificity for PID diagnosis. au 3 2003 re-analysis data by Simms et al., the combination Tever (temperature >38.3 C), elevated ESR, and adnexal | tenderness achieved the hi itivi ifici ighest sensitivity and specificity, 65 and 66%, re Pr | respe salpingitis. Ctively, for acute s ‘dapece post Potential gold standards for a true postive jndometrial biops Salpingitis at laparoscopy or endometritis © jand not part of. » an ecause laparoscopy is expensive, invas |endometritig a standard evaluation of PID, many studies : ~———e 8 marker of upper Genital tract infection 2 Scanned with CamScanner'and inflammation. | Endometritis and salpingitis are correlated; histologic |endometritis has sensitivity of 89% to 92% and specificity of 63% to 87% for laparoscopically diagnosed acute salpingitis, with only 7% to 22% of patients with clinically suspected PID ‘having salpingitis without endometritis. | Reference | Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2015. | MMWRR 2015; 64 (3):1-140. CDC 2015 | Mitchell C, Prabhu M. Pelvic Inflammatory Disease Current Concepts in Pathogenesis, , | Diagnosis and Treatment. Infect Dis Clin N Am 27 (2013) 793-809 Scanned with CamScannerDIAGNOSTIC EVALUATION Analyn F. Fallarme, MD Henrietta S. Lucasan, MD/Maria Lorena L. Santos, Mp No single historical, physical, or laboratory finding iS reliab | diagnostic for acute PID. We are therefore left with the Challenge of diagnosing PID in such a way as to minimize its associate | sequelae while at the same time not over treating all women with pelvic pain or other genital tract symptoms with antimicrobials, ‘Nonetheless, a number of procedures can be Performed to ‘improve the diagnosis of pelvic inflammatory disease (PID) and its complications, and these includes: | 1. Laboratory testing (WBC count, wet mount, ESR, CRP) 2. Imaging studies (ultrasound, CT, MRI) 3. Laparoscopy STATEMENT: ‘PID is a clinical diagnosis, blood cell count, ESR, CRI necessary, but can be h in defining its seve: ity. Supporting Statements: ‘In the PID Evaluation {enrolled women with hence, laboratory data (white P, saline wet mount) are not usually elpful in establishing the diagnosis | However, only 60% of patie i ith serum WAC count Patients with PID present wi 4 Scanned with CamScanner‘ESR, a nonspecific inflammatory marker has been found to be elevated in PID but an elevated ESR (> 15 mm/h) is only present ‘in approximately 75% of women with acute PID and, as a nonspecific marker of inflammation, can be found in other disease states. In another cohort study (Piepert, 1996), an ‘elevated ESR (>15 mm/h) had 70% sensitivity and 52% ' specificity for endometritis or salpingitis. ‘CRP, another inflammatory marker, has been studied in acute PID. Ina series that involved 152 patients, a CRP > 10 mg/dL had ‘a good sensitivity (93%) and specificity (83%) in the diagnosis of PID (Hemila et al, 1987). Furthermore, CRP levels decrease to normal sooner than ESR following effective antibiotic therapy and | may be beneficial as a monitoring tool. The presence of 1 or more neutrophils per 1000/field saline wet mount of vaginal discharge had 91% sensitivity and 26.3% specificity for endometritis. In a cohort of women (Yudin et al, 2006) at high risk for pelvic infections, absence of vaginal WBCs had excellent negative predictive value (95%). These data suggest that if an evaluation of a saline microscopy of vaginal fluid reveals no WBCs (leukorrhea), an alternative diagnosis to. PID should be considered. | [Table 1; Summary of the sensitivity and specificity values of different laboratory tests used in the diagnosis of PID. Author Test Sensitivity | Specificity | Soper, 1991 Leukocyte count >10,000] 41% 76% . cells/mL. Piepert, 1996 | ESR>15 mm/h 70% 52% Hemila et al, [ CRP > 10 mg/dL 93% 83% 1987 Aneel et al,| Presence of 21 neutrophils| 91% 983 per 1000/field saline wet mount of vaginal discharge 26.3% Scanned with CamScannerin the diagnosis and treatment of po), lc Refer i i hr ences iderations consi { North America, vol. 71, no. 5, pp. 947-969 “Surgical mn nay aaa" Surgical Clinics of 1991. Hemila M, Henrikson Land A i of peli inflammatory disease,” Arch 182, 1987. ; i 9. BP TT tae Washinglon AE, a al. Diagnosing pelvic inflammatory disease, Comprehensive analysis and considerations for developing a new model, JAMA 1961, '18):2594-604. ith Fe eres RB, She J ta. Circa predictors of endometris in women wih Symptoms and signs of pelvic inflammatory disease. Am J Obstet Gyneco! 2001; 184(6):856-63 (discussion: 63-4]. ; vedir MH, Hillier SL, Wiesenfeld HC, et al. Vaginal polymorphonuclear leukocytes ang actorial vaginosis as markers for histologic endometritis among women without symptoms of pelvic inflammatory disease. Am J Obstet Gynecol 2003; 188(2):318-23. Peipert JF, Boardman L, Hogan JW, et al. Laboratory evaluation of acute upper genital tract infection. Obstet Gynecol 1996; 87(5 Pt 1):730-6. ‘Amsel R, Totten PA, Spiegel CA, Chen KC, Eschenbach D, Holmes KK. Nonspecific itis: diagnostic criteria and microbial and epidemiologic associations. Am J Med ikorkala , “Serum CRP in the diagnosis and treatment ives of Gynecology and Obstetrics, vol, 241, no, STATEMENT: A transvaginal ultrasound is recommended in all cases of PID to aid in the diagnosis and treatment approach. If classic findings of PID are noted on ultrasound, no further imaging is required. If additional characterization is warranted, MRI recommended over CT because its overall accuracy e greater than 93% and does not carry the additional risk of ionizing radiation. Rupporling Statements: iD trasonography can also be used i i is of sono to aid in the diagnos! te = rect treatment. A finding of thickened, fluid-filed tube 6 sensitivity and 100% specificity for endometrtis ™ women with clinically diagnosed PID, ; ind! sonata and colleagues detalled the various tansv@®"” graphic markers of acute tubal inflammatory diseas® | Scanned with CamScannereS ‘including: \, dilated tubal shape, » abnormal wall structure, » increased wall thickness (>5 mm), and presence of pelvic peritoneal fluid (free fluid or inclusion cyst), ‘In a prospective study of 51 women with suspected PID ‘Cacciatore et al. demonstrated that a transvaginal sonogram ‘suggestive of PID, e.g., thickened, fluid-filled tubes, had a | sensitivity of 85% and a specificity of 100% for the diagnosis of | plasma cell endometritis as determined by an endometrial biopsy. ‘The positive and negative predictive values for the group were 400 and 95%, respectively. The authors concluded that transvaginal sonography can aid in the outpatient evaluation of ‘women with suspected PID. ‘in a study (Molander et al, 2003) comparing 30 patients with ‘clinical PID confirmed with laparoscopy and 20 normal women, ‘power Doppler demonstrating tubal hyperemia was 100% ‘sensitive and 80% specific for PID; in addition, altered tubal ishape, structure, and wall thickness were seen in an ‘overwhelming majority of patients with pyosalpinx. i Although the literature is replete with reports regarding the sonographic findings of PID, little was published about CT images until the last decade. CT findings in early PID include: + obscuration of the normal pelvic floor fascial planes, + thickening of the uterosacral ligaments, * cervicitis, oophoritis, salpingitis, and 7 : lation imple fluid in the endometrial canal, The simple fluid may become complex as the disease progresses and eventually become a frank tubo-ovarian or pelvic a | Reactive inflammation can manifest as small or large bowel ileus | or aa 7 _ and right r hydronephrosis or and rig q : $ vegonenhetl r tis syndrome). One i _Intian ae nn drawback of CT images however is the exposure to ionizing ‘adiation, which can be problematic in young women. Scanned with CamScannerjmaaing, with its highly sensitive and g, Magnetic resonans ened, fui-filed tubes, pyosalpinx, ability to Cones ovarian abscess (TOA), has also bene free as aa diagnostic modality for PID; however, it is os Sand not easily accessible or applicable to women seek outpatient evaluation for possible PID. PECific Pelvig mpared transvaginal ultrasonography, MRI, an wee yin 30 in-patients hospitalized in Finland with cliicaly suspected PID and reported that MRI diagnoses were 95% correct in 21 women with laparoscopically-proven acute salpingitis compared with transvaginal sonogram that was 81% accurate. The sensitivity of MRI in the diagnosis of PID was found to be 95%, with a specificity of 89%, and overall accuracy was 93%. For transvaginal US, the corresponding value was 81%, 78%, and 80%, respectively. MRI is more accurate than transvaginal US and provides information about the differential diagnosis of PID, and as such its use may also reduce the need for diagnostic laparoscopy. Table 2: Summary of the sensitivity and specificity values of different imaging studies used in the diagnosis of PID. Author Test Sensitivity | Specificity Cacciatore et al, 1992 Ultrasonography 85% 100% Molander et al, 2003 Doppler study 100% 80% Tukeva et al, 1999 MRI 95% 89% References - / Cacciatore B, Leminen A, Ingman-Friberg S, et al. Transvaginal sonographic findings in ambulatory patients with suspected pelvic inflammatory disease. Obstet Gynecol 1992; 80(6):912-6, Timor-Tritsch IE, Lerner JP, Monteagudo A, et al. Transvaginal sonographic markers © , tubal inflammatory disease. Ultrasound Obstet Gynecol 1998; 12(1):56-66. | Molander P, Finne P, S| 7 joberg J, et al. Observer agreement with laparoscopic diagnos” of pelvic inflammatory di is - tik ‘ 675-80. 'sease using photographs. Obstet Gynecol 2003; 101 (6 | Peipert JF, Soper DE. Diagnostic Evaluation Se. Infections iseasen, 7 of Pelvic Inflammatory Diseas i ueanes in Obstetrics and Gynecology 1994; 2: 38-48, Mr ny: ,/200bs JE, Bimbaum BA. Spectrum of CT Findings in Acute Pyoge" Inflammatory Disease. RadioGray . hi ; 22 (6): 1327- Tukeva TA, Aronen Hi, Karalainen Pet a; roe comparison with laparoscopy jc Pawo east! en PT, ot al. MR imaging in pelvic. inflammatory 4 and us. Radiology 1999; 210 (1): 209-16. Scanned with CamScannerye ce EE coey Laparoscopy the criterion standard for the dia: | Pasar gnosis of |pID, and is sign! icantly more specific and sensiti clinical criteria alone. ensitiveithan|are ie minimum criteria for diagnosing PID laparoscopically include: ' pn’ tubal wall edema, " Visible hyperemia of the tubal surface, and the | the tubal surfaces and fimbriae. | |. presence of exudate on | Supporting Statements: hown to add considerable accuracy to) | Laparoscopy has been sl |the clinical methods of diagnosing acute salpingitis. | The) | procedure does not aggravate the inflammatory process. | Jacobson and Westrom looked at 905 cases over an eight-year | |period (1 960-1967) and set the standard for laparoscopic | | diagnosis. The minimu ic criteria for visual diagnosis | of acute salpingitis include: pronounced hyperemia of the tubal | | surface, edema of the tubal wall, and, thirdly, a sticky exudate on; the tubal surface and from the fimbriated ends when patent. In) their study, they hardly encountered difficulties differentiating | |mild pathologic changes and normal conditions, but one major | drawback that can be envisaged is the patient with endometritis | ‘who has no salpingitis. In 814 cases in their series with | | Suspected acute PID, 532 (65%) had laparoscopically confirmed | jpoute salpingitis, 12% had other pathologic conditions, and 23% | |had no pathologic conditions changes. clinical and lal te PID, Eschen! boratory findings with | bach and coworkers | ity of clinical and laboratory | exal mass) was not associated | and that the severity of some: d negatively with the severity of | le another study comparing |ereeconic findings of acu’ lgeee eee the severi eee (other than adn “find ively with tubal occlusion ndings was actually associate tubal damag Scanned with CamScanneris referred to as the “gold standard” for the Atnoug ey PID, review of the literature regarding its accuracy has been mixed. Accuracy of a clinical diagnosis when cCompareq with diagnostic laparoscopy In the diagnosis of PID has been reported in various studies. Morcos et al. in a study of 176 women with clinically diagnosed PID established laparoscopically confirmed PID in 76.1% of the cohort. Similarly, Cohen et al. ina prospective case-control study investigated the etiology Of acute salpingitis in a cohort of Kenyan women and confirmed Salpingitis laparoscopically in 142 (90%) of the 158 women with a clinical diagnosis of acute PID. Conversely, Peipert et al. found the sensitivities of both the accepted clinical criteria and the triad of laparoscopy visualization of edema,erythema and purulent exudates to be low. In that study, the sensitivities of the CDC’s minimal clinical criteria for PID and the laparoscopic triad of edema, erythema, and purulent exudates were 65% and 60%, respectively. Sellors et al. also found laparoscopy to be 50% and 80% sensitive and specific, respectively. In this study, additional evidence from endometrial and fimbrial biopsy increased the prevalence of confirmed PID from 30% in visual diagnosis alone to 46% when endometrial and fimbrial mini-biopsy evidence was included. Women with a recurrent diagnosis of PID and persistently negative NAATs and who are classified as “lower risk" epidemiologically should have laparoscopy to consider alternative diagnoses such as endometriosis. ‘The main drawbacks of laparoscopy are that the procedure e expensive and invasive, exhibits inter-observer variability, 2" requires an operating room and anesthesia. In addition, findings on laparoscopy do not necessarily correlate with the severity © illness, in that only the surfaces of structures are visible throug , the scope. References: . 2 seas" ree ita L. Objectivized diagnosis of acute pelvic inftammator) ps 1088-1098, 10 roomate value of routine laparoscopy. Am J Obstet GY" Scanned with CamScannerFeschenbach DA, Wolner-Hanssen P, Hawes SE, P; | Ke “acute pelvic inflammatory disease; ancocieiona of cine, S i cepted | laparoscopic findings,” Obstetrics and oratory findings yah ee Gynecology, vol, 89, no, 2, pp. 184-192, | Morcos R, Frost N, Hnat M, Petrunak A, and Caldito G. ‘diagnosis of acute pelvic inflammatory disease," ‘vol. 38, no. 1, pp. 53-56, 1993, ‘cohen CR, Mugo NR, Astete SG, et al. “Detection of mycoplasma genitali women with laparoscopically diagnosed acute salpingitis,” Sexualy Transmitted ‘Infections, vol. 81, no. 6, pp. 463-466, 2005. \Peipert JF, Boardman LA, and Sung CJ, “Performance of clinical and laparoscopic ‘criteria for the diagnosis of upper genital tract infection,” Infectious Diseases in ‘obstetrics and Gynecology, vol. 5, no. 4, pp. 291-296, 1997. | Sellors JW, Mahony J, Goldsmith C, et al., “The accuracy of clinical findings and laparoscopy in pelvic inflammatory disease,” American Journal of Obstetrics and | Gynecology, vol. 164, no. 1 |, pp. 113-120, 1991. | Molander P, Finne P, Sjoberg J, Sellors J, Paavonen J. Observer agreement with | ‘laparoscopic diagnosis of pelvic inflammatory disease using photographs. Obstet | Gynecol. 2003 May. 101(5 Pt 1):875-80. “Laparoscopic versus clinical Journal of Reproductive Medicine, » | STATEMENT: J / One of the most specific criteria for diagnosing PID includes | ‘endometrial biopsy with histopathologic evidence of) Supporting Statements: / sveny'iiy the .Endometrial biopsy has been studied extensively in diagnosis of PID. It is less invasive compared with percent The presence of neutrophils and plasma cells in ae [endometrium is indicative of endometritis and may be uso 4 PID. Endometrial biopsy is approximately | % sensitive. Endometrial biopsy is approximately 90% specific and 90% Sensitive Scanned with CamScanner: ‘ed at endometrial histopathology in g9 Kivat and a cepacia acute PID and reported that boy the patients had both upper genital tract infection (UGT) and laparoscopically confirmed salpingitis. They reported UGT] without salpingitis in 1%, while salpingitis without UGTI was. reported in 16%. The study found that the simultaneous presence of five or more neutrophils per X400 field in endometria| surface epithelium, together with one or more plasma Cells per X120 field in endometrial stroma were the best predictor of upper genital tract infection plus salpingitis. This combination had a sensitivity of 92% and a specificity of 87% for Predicting the diagnosis of both UGTI and laparoscopically confirmed acute salpingitis. Additionally, 90% of all UGTIs identified in this study were attributable to C. trachomatis or N. gonorrhoeae, and 92% | of the women diagnosed with UGTI and salpingitis had either! chlamydia or gonorrhea infection. Current CDC guidelines recommend endometrial biopsy in women undergoing laparoscopy who have no visible signs of salpingitis, on the grounds that endometritis may be the only sign | of PID. Diagnostic use of endometrial biopsy in the emergency department is limited; significant operator training is required, and the results of the procedure are not immediately available to the ‘clinician. ‘Endometrial biopsy findings usually confirm the presence of ‘infection but rarely identify the causative organism. Chronic: _endometritis is more commonly seen than acute endometriti | References _ Kiviat NB, Wolner-Hanssen P, Eschenbach DA et al., “Endometrial histopathology i" Patients with culture-proved upper genital tract infection and laparoscopical diagnosed acute salpingitis,” Ameri i 414, no. 2s PP 167-175, 1990. gi ican Journal of Surgical Pathology, vol. 14, | Workowski KA, Berman S. Sexually idelines, 2015 | : J ly transmitted diseases treatment guidelines, MMWR Recomm Rep 2015; 64 @):1-140, : Scanned with CamScannerMANAGEMENT Josefa Dawn V. Martin, MD Sybil Lizanne R. Bravo, MD/Maria Lu D. Andal, Mp STATEMENT: Out-patient therapy can be considered in women with mild to moderately severe pelvic infection. The clinical outcomes of women given oral and parenteral regimen appear to be similar. Supporting Statements: The Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) trial compared in-patient administration of parenteral cefoxitin and doxycycline (parenteral/oral) with outpatient administration of intramuscular cefoxitin and oral doxycycline (Ness at al, 2002), and found no short-term (30-day) differences in microbiologic or clinical cure or long-term differences in reproductive health outcomes (Table 1). Table 1: Summary of short-term and long-term effects of out-patient compared with in-patient therapy for mild to moderate PID in the PEACH trial Outpatient (%) | Inpatient (%)__| P value Short term (30d) _ Gonorthea positive 3.9 24 44 Chiamydia positive 27 3.6 52 Persistent tenderness 20.6 18.4 50 Endometritis 45.9 37.6 09 Longterm (mean 35 mo) Pregnancy 59.4 55.6 NS Ectopic 12 0.2 NS. Infertility 16.7, 20.6 NS Chronic pelvic pain 40.7 44.6 NS Recurrent PID. 18.4 24.3 NS ; 3S A secondary analysis among participants of the PEACH wil (6 et al, 2005) also found no long-term outcome different ned treatment group among those with clinically-COn ia endometritis or upper genital tract gonorrheal or chia Scanned with CamScanner, oon. yf interest, a representative sub) i ijptection- fe) subpopulation from PEAC! oe aied a 70% mean treatment adherence rate, with only 17% 4 ‘reveal ., ; paricipants taking doxycycline exactly as prescribed. Similar tes of poor adherence to doxycycline or tetracycline prescribed utpatient therapy for sexually transmitted infections (STIs) have been seen, particularly in the setting of gastrointestinal side effects. This finding may explain the relatively high rates of ongoing disease and long-term sequelae in the PEACH cohort. for 0! reas many of the original efficacy studies mandated inpatient nous treatment of 48 to 96 hours before switching to oral therapy, current practice is to treat with intravenous medications until there is clinical improvement for 24 hours or more. However, because intravenous doxycycline can cause significant phlebitis and its oral bioavailability is comparable with that of parenteral bioavailability, an earlier switch to oral doxycycline can be made if a patient is tolerating oral medications. ‘hel intraver References Ness RB, Soper DE, Holley RL, strategies for women with pelvic inflammator inflammatory Disease Evaluation and Clinical Health (PEACH) rant Obstet Gynecol 2002;186 (5):929-37. ‘Ness RB, Trautmann G, Richter HE, et al women with pelvic inflammatory disease: a randomized tri (573-80. Dunbar-Jacob J, Sereika SM, Foley SM, et al. Adherence to oral therapies in pelvic inflammatory disease. J Womens Health 2004; 13 (3):285-91. Augenbraun MH, McCormack WH. Pelvic inflammatory disease: an ongoing epidemic. Hosp Pract (1995) 1995; 30 (9):61-6. Katz BP, Zwick! BW, Caine VA, et al. Compliance with antibiotic therapy for Chlamydia \achomats and Neisseria gonorrhoeae. Sex Transm Dis 1992; 19(6):351-4. come DL, Little BB, Faro S, et al. Comparison of three regimens recommended by the Saag for disease control and prevention for the treatment of women hospitalized with _S2ute pelvic inflammatory disease. Clin Infect Dis 1994; 19 (4):720-7. et al. Effectiveness of inpatient and outpatient treatment ry disease: results from the Pelvic: domized trial. Am J |. Effectiveness of treatment strategies of some ial. Obstet Gynecol 2005; 106 n regarding the need for judgment of the | t meets any of the | STATEMENT: The de Spitalization should be based on the “care provider and whether the patien “Suggested criteria for hospitalization : Scanned with CamScannering Statements: . : Shee tne 1980s, PID therapy has shifted from the inpatient to the outpatient setting, with a 68% decline in hospitalization attributable in part to several studies showing equivalent short. term outcomes with outpatient versus inpatient therapy for milq to moderate PID. Between 1995 and 2001, 89% of all PID Visits occurred in the ambulatory setting. Current criteria for in-patient hospitalization are summarized in Table 2. Table 2: Criteria for in-patient management of PID Surgical emergencies cannot be ruled out Pregnancy Lack of clinical response to oral antimicrobial PID therapy after 72 hours | Inability to tolerate or comply with out-patient management Severe illness, high fever, nausea, or vomiting Presence of tubo-ovarian abscess The PEACH study demonstrated that in women with mild-to- | Moderately severe PID, outpatient oral therapy results in similar short- and long-term clinical outcomes as inpatient therapy. If none of the conditions mentioned above are Present, then the Patient may be managed initially as an outpatient. However, outpatients should be reevaluated within three days, and if there is no improvement, then inpatient Parenteral therapy should be instituted, Limited studies have demonstrated that Pregnant women with PID have high rates of fetal wastage and preterm delivery, supporting the appropriateness of hospitalization. Similarly, data supports hospitalization of women with TOAs in order to maximize antimicrobial dosing and close monitoring for early recognition of ‘Scanned with CamScanner——— Le [Several previous criteria for hospitalization hav “removed | ifrom the current suggestions. The seeeeatch tata doers | ‘penefit from hospitalization for adolescent girls with PID ted tha ‘CDC to not list adolescence among the criteria for hospitalization ‘and to suggest that a decision to hospitalize adolescents with PID should be based on the same criteria used for older women. | References Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment ‘strategies for women with pelvic inflammatory disease: results from the Pelvic | |jnflammatory Disease Evaluation and Clinical Health (PEACH) randomized trial. Am J | Obstet Gynecol 2002;186 (5):929-37. i | Ness RB, Trautman G, Richter HE, et al. Effectiveness of treatment strategies of some | gornen with pelvic inflammatory disease: a randomized trial. Obstet Gynecol 2005; 106 ! | @);573-80. |Dunbar-Jacob J, Sereika SM, Foley SM, et al. Adherence to oral therapies in pelvic | inflammatory disease. J Womens Health 2004; 13 (3):285-91. | |Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2015. | MMWR Recomm Rep 2015; 64 (3):1-140. i Statement: Treatment of pelvic inflammatory disease should | provide high rates of clinical and microbiological cure for a_ | ange of pathogens and should ultimately prevent |teproductive morbidity. t \ | ‘Scanned with CamScanner3: Outpatient Regimen oe ed Intramuscular/Oral Regimens Cefoxitin 2 g IM in a single dose and Probenecid, 1 @ oraly administereg i Metronidazole 500 mg orally twice a day for 14 days _ coverage of macanes eee an capers uence anerbe Sean's Sinan Scere ee to pat Senge fo Diseases Treatment Guidelines. Cin Infect Dis 2007:25(S4P = " zal . Bolan, GA, et al; Centers for Disease Co! and Prevention. Sexually o 2018 : Transmitted Diseases Treatment Guidelines. MMWR Recomm Rep .2015:64(No. RR-3): 81 an ~ — ae hd us ity of oral probenecid in the Philippines preclud?. 2 xi from using the Outpatient regimen involving single dose oot and Oral Probenecid and oral doxycycline. ‘Scanned with CamScannerTable 4: In-patient Regimen _ _ [Recommended Parenteral Regimens ‘PLUS os {Doxyeyefine 100 mg orally or IV ev Adapted from Workowski KA, Bolan, GA, et al; Centers (rol Prevention. Sexually Transmitted Diseases Treatment Guidelines, 2015. [MMWR Recomm Rep 2015;64(No. RR-3): 80 Alternative Parenteral Regimen _ (Clindamycin_ plus gentamicin, cefoxitin plus doxycycline, and Cefotetan plus doxycycline have shown to provide very good Short-term clinical and microbiological efficacy. Oral therapy for acute PID is currently the most commonly used approach, in Tesponse to both economic issues and the evidence from the Fo ‘CH study demonstrating that both short-term and long-term “tqomes were similar for the oral and paren Due the increased ne resistance of N. gon choices juinolone resistance g oe (Of oral regimens are ie d. Ceftriaxone or cefoxitin ' “Gemonstrated excellent short-term clinical and microbiological aults, The addition of oral metronidazole to this regimen is | SUggested by some experts to provide improved anaerobic in nage and at least to treat Bacterial vaginosis which is present ® t0 70% of women with acute PID. ‘Scanned with CamScannerfor gonorrhea, and therefore PID, shifted away Tree notone-based regimens between | the 2006 and 2010 iterations of the CDC Treatment Guidelines, given the rapig emergence of fluoroquinolone resistance. In 2012, after reports of increasing prevalence of cefixime-resistant gonorrhea, the guidelines were changed again to drop cefixime as one of the first. line outpatient treatment options for cervicitis. With addition cephalosporin resistance to gonorrhea reported, the potential for development of resistance that could compromise treatment of gonorrhea-associated PID is of great concern. from Resistance to ciprofloxacin has become widespread throughout many parts of Asia. Rapid emergence of high-level resistance ina high proportion of gonococcal isolates during a 2-year period (1994-1996) has now been documented in the Philippines, and continued spread of highly resistant isolates is likely (de los Reyes, 2001). This randomized trial documented an unacceptably high rate of failure (45%) after patients received ciprofloxacin treatment for cervical infections caused by gonococci with high-level ciprofloxacin resistance. Hence, Ciprofloxacin is no longer @ useful drug for treatment of gonorrhea in the Philippines. "Among patients who qualified for outpatient therapy, re-evaluation of clinical status should occur within 72 hours, or sooner ‘ indicated. If no meaningful clinical response is detected, pation with PID may require inpatient hospitalization, transition parenteral antibiotics, further diagnostic tests including addition laboratory studies and imaging to evaluate for possible TOA, Possible surgical intervention. ial In a meta-analysis (Walker, et al, 1993) of 34 treatment ue Published primarily between 1985 and 1992, 4 inpatient rea ru and 1 outpatient regimen were found to have pooled clinical 168 rates ranging from 92% to 95% and microbiological CU"? juded ranging from 91% to 100%. These in-patient regimens in¢ _the following drugs: ‘Scanned with CamScannerAntibiotic Regimen Clinical Cure Rate Gindamycin & Aminoglycoside 92% Merobolgiy Cure Fae | Cefoxitin & Doxycycline 93% 98% Cefotetan & Doxycycline 94% 100% Ciprofloxacin 94% 96% ‘Metronidazole & Do» ine 75% 71% |The low efficacy rates for the last regimen are likely attributable to ‘the poor coverage of this combination against N. gonorrhoeae. ‘One outpatient regimen (cefoxitin, probenecid, and doxycycline) | ‘was included in this meta-analysis and was found to have a. pooled clinical cure rate of 95% and a microbiological cure rate of | 191%. ‘Also of interest because of its association with enhanced) ‘compliance, single-dose or short-duration azithromycin in the’ ‘treatment of PID has been examined in a handful of studies | (Rustomjee et al, 2002). Not surprisingly, compliance with single- | ‘dose azithromycin therapy has been reported to be 100%. ‘Although not part of the CDC recommendations, newer data’ “Suggest that parenteral followed by oral azithromycin, either as | ‘Monotherapy or in combination with doxycycline and: ‘metronidazole, produces clinical cure rates of 97% to 98% at 2 | weeks after initiation of treatment, and microbiologic cure rates of 90% to 94% at 6 weeks post-treatment (Bevan et al, 2003). The, |azithromycin-based regimens were compared with third-, \9eneration cephalosporin-based regimens or parenteral | Amoxicillin-based regimens and showed no statistically significant | difference in clinical or microbiologic cure rates, although the, ly had a high drop-out rate and low proportion of anaerobic . eria isolated from endocervix and endometrium. : (other trial compared intramuscular ceftriaxone plus oral, “hig hromycin with the standard of oral doxycycline, and found’ |athog fates of clinical and histologic cure with azithromycin, | 07) rates of cure in both arms were less than 80% (Savaris et | ‘Scanned with CamScanner