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PID lecture by Associate Professor Dr Aisha Elbareg

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PID lecture by Associate Professor Dr Aisha Elbareg

  1. 1. Pelvic Inflammatory Disease (PID) Associate Clinical Professor Dr. Aisha M. Elbareg, MBBS, DGO, MMedSci., ABOG, MD, PhD. Senior Consultant in (Obs & Gyn) and Reproductive Medicine Faculty of Medicine, MisrataUniversity. LIBYA aishaelbareg@med.misuratau.edu.ly 2019
  2. 2. Overview History:  A relation between gonorrhoeae, pelvic inflammatory disease, and tubal infertility was generally apparent in the preantibiotic era. In 1879, Neisser discovered the gonococcus, and named after him (Neisseria Gonorrhoeae), which became linked with adnexitis soon thereafter, upper genital tract infection and severe tuboovarian abscess was feared to be associated with gonococcal infection.  With availability of penicillin in the 1940s, both lower and upper genital tract infections could be more effectively treated, and the effects of their sequelae were felt to be lessened.  In the 1960s, Swedish Investigators laid the cornerstone for measuring the impact of STDs on subsequent tubal infertility, importance of chlamydia as a cause of tubal infertility, different risk factors on fertility prognosis, and the effects of different antibiotic regimens.  During 1970s, the role of Chlamydia trachomatis in PID became increasingly appreciated.  In recent years, the nature of pathophysiological process of PID became increasingly understood, eventually its management.
  3. 3. Overview  (PID) is usually the result of infection ascending from the endocervix, (intercourse may contribute to the ascent of infection through rhythmic uterine contractions occurring during orgasm), causing a spectrum of inflammatory disorders of the upper female genital tract including any combination of : Endometritis, Salpingitis, Parametritis, Oophoritis, Tuboovarian Abscess(TOA) and/or pelvic Peritonitis, {in addition to perihepatic structures (Fitz-Hugh−Curtis syndrome)}. Incidence steadily increased in 1970s due to rising rates of STDs and peaked in early 1980s. The annual rate of PID in high-income countries has been reported to be as high as 10-20 per 1000 women of reproductive age. It could be acute, subacute, recurrent, or chronic.  Genetically mediated variation in immune response plays an important role in susceptibility to PID. Variants in the genes that regulate toll-like receptors (TLRs), an important component in the innate immune system, have been associated with an increased progression of C trachomatis infection to PID.
  4. 4. Overview Causative agents: (PID is polymicrobial): Chlamydia trachomatis, an intracellular bacterial pathogen is the predominant sexually transmitted organism associated with PID (50-65%), other organisms include : Neisseria gonorrhea, (15-30%), more often produces more acute symptomatic disease, Gardnerella vaginalis (which causes bacterial vaginosis (BV), Mycoplasma hominis, Ureaplasma urealyticum, Trichomonas vaginalis, Haemophilus influenzae, and anaerobes such as Peptococcus and Bacteroides species, Non- hemolytic streptococcus, E. coli, Group-B streptococcus & staphylococcus. An estimated 10-20% of untreated chlamydial or gonorrheal infections progress to PID.
  5. 5. Overview : Mode of transmission Through uterine lymphatics & blood vessels across parametrium Mycoplasma probably spreads across the parametrium to affect the tube
  6. 6. Chlamydia trachomatis Neisseria gonorrhea Neisseria gonorrhea Haemophilus influenzae Pe Peptococcus Bacteroides PID is polymicrobial Ureaplasma urealyticum Trichomonas vaginalis Mycoplasma
  7. 7. Overview Factors associated withPID :  (Those related to sexual behaviours): Young age: {because of increased cervical mucosal permeability, a larger zone of cervical ectopy, a lower prevalence of protective antichlamydial antibodies, and increased risk-taking behaviors}., multiple partners, recent new partner, past history of sexually transmitted infections in the patient or their partner. Others: Instrumentation of the uterus/interruption of the cervical barrier, termination of pregnancy, insertion of intrauterine device within the past three-six weeks ( linked to a 2- to 9-fold increased risk ), hysterosalpingography(HSG), hysteroscopy, saline infusion sonography & IVF. Frequent vaginal douching has been considered a risk factor for PID, but studies reveal no clear association.
  8. 8. Overview Protective factors associated with PID: Barrier methods: Specially condom with spermicidal chemicals, Oral steroidal contraceptives: -Thick mucus plug (preventing ascent of sperm and bacterial penetration, decreasing menstrual anterograde and retrograde flow, and modifying local immune responses), Tubal ligation, Uncommon in women who are not menstruating, Pregnancy. Tubal ligation
  9. 9. Pathology:  Involvement of the tube is almost always bilateral and usually following menses due to loss of genital defense.  Pathological process is initiated primarily in the endosalpinx.  There is gross destruction of the epithelial cells, cilia and microvilli and may becomes edematous and hyperemic (in severe infection).  The exfoliated cells along with the exudate pour into the lumen of the tube and agglutinate the mucosal folds. The abdominal ostium is closed by the indrawing of the edematous fimbriae and by inflammatory adhesions, uterine end is closed by congestion. Closure of both the ostia results in built up of the exudate inside the tube. The exudate may be watery producing hydrosalpnix (Acute catarrhal salpingitis, Serous fluid, thin wall, mild adhesions) or purulent producing pyosalpinx, (suppurative salpingitis, thickened tube, full of pus, dense adhesions ), which changes the microenvironment and favors growth of other organisms resulting in deeper penetration and more tissue destruction.
  10. 10. Pathology:  There will be adhesions of the tube with the surrounding structures.  On occasions, the exudate pours through the abdominal ostium to produce pelvic peritonitis and pelvic abscess or may affect the ovary producing ovarian abscess.
  11. 11. tuboovarian abscess& Hydrosalpnix
  12. 12. Acute Salpingitis with abundant inflammatory infiltrate/pus in the Lumen
  13. 13. Clinical features of PID Clinical Features
  14. 14.  PID may be symptomatic or asymptomatic. Clinical symptoms and signs lack sensitivity and specificity (the positive predictive value of a clinical diagnosis is 65–90% compared to laparoscopic diagnosis).  Symptoms usually appear at the time and immediately after the menstruation.  Bilateral lower abdominal and pelvic pain which is dull in nature, aching or crampy, and constant; tends to be accentuated by motion, exercise, or coitus.  Rebound lower abdominal tenderness and involuntary guarding may be noted and suggest associated peritonitis.  Fever (>38°C found in 30% of cases), lassitude and headache.  Irregular and excessive vaginal bleeding, often postcoital, is reported in about 40% of cases, is usually due to associated endometritis.  Abnormal vaginal discharges present in approximately 75% of cases which becomes purulent and or copious. Clinical features:
  15. 15. Clinical features:  Nausea and vomiting, manifest late in the clinical course of the disease.  Deep dyspareunia.  Pain and discomfort in the right hypochondrium due to concomitant perihepatitis (Fitz-Hugh-Curtis syndrome) may occur in 5–10% of cases of acute salpingitis  Congested external urethral meatus or openings of Bartholin’s ducts through which pus may be seen escaping out on pressure.  Vaginal speculum examination shows congested cervix with purulent discharge from the canal.  Bimanual examination reveals bilateral tenderness on fornix palpation, which increases more with movement of the cervix. There may be thickening or a definite mass felt through the fornices.
  16. 16. Differential diagnosis:  The differential diagnosis of lower abdominal pain in a young woman includes:  Acute appendicitis.  Ectopic pregnancy.  Urinary tract infection/Interstitial cystitis.  Diverticulitis.  Endometriosis.  complications of an ovarian cyst, i.e. rupture, torsion.  Adnexal tumors  Cholecystitis.  Functional pain (pain of unknown physical origin).
  17. 17. Differential diagnosis of Acute PID: (Acute appendicitis and disturbed ectopic pregnancy, (MOSTCOMMON), must be ruled out, because both conditions require urgent laparotomy)!! DD Acute salpingitis Symptoms and signs Acute Salpingitis Acute Appendicitis Disturbed ectopic Pregnancy
  18. 18. Differential diagnosis of Acute PID: Torsion Ovarian cyst:  Sudden pain in the abdomen  Occasional vomiting.  Pyrexia usually absent  No menstrual irregularities  Vaginal discharge absent.  Tender abdominal Lump.  Ultrasound: confirm Ruptured Endometriotic Cyst:  Patient is afebrile.  No vaginal Discharge.  Dysmenorrhea, menorrhagia, and pelvic pain before acute episode.
  19. 19. Differential diagnosis of Acute PID:  Cholecystitis:  History of flatulent dyspepsia.  Severe pain in the right hypochondrium radiating to the top of right shoulder.  Nausea and vomiting with fever.  Pain, jaundice, and rigor.  No Vaginal discharge.  Menstrual irregularities absent. Diverticulitis.  Usually occurs after the age of 50 years.  Infection Signs confined to left iliac fossa.  No Vaginal discharge.  Menstrual irregularities absent.
  20. 20. Clinical diagnostic criteria of PID: o MinimumCriteria:  Adnexal tenderness.  Cervical motion tenderness.  Uterine tenderness. o Definitive Criteria:  Endometrial biopsy with histopathological evidence of endometritis.  Transvaginal sonography or magnetic resonance imaging techniques showing thickened, fluid-filled tubes with or without free pelvic fluid or tubo-ovarian complex, or Doppler studies suggesting pelvic infection (e.g., tubal hyperemia).  Laparoscopic findings consistent with PID. o Additional Criteria:  Temperature (>38.3°C).  Abnormal cervical mucopurulent discharge or cervical friability.
  21. 21. Clinical diagnostic criteria of PID: o Additional Criteria:  Presence of abundant numbers of WBC on saline microscopy of vaginal fluid.  Elevated ESR, Elevated CRP(supports the diagnosis but is non-specific and often normal in mild/moderate PID).  laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis. Investigations:  A pregnancy test to exclude, the possibility of ectopic pregnancy.  High vaginal and endocervical swabs, should be sent for aerobic, anaerobic culture, drug sensitivity testing and gram stain.  Midstream specimen of urine for microscopy and culture.  Full blood count and C-reactive protein, and total bio.  Serological test for syphilis for both partners.  Ultrasound might be useful to confirm pelvic abscess, hydrosalpinx, and (TOAs), while (CT) or {MRI, has relatively high specificity (95%) and sensitivity (95%)}, it can help rule out other causes of peritonitis.
  22. 22. Ultrasonographic findings in PID may include the following:  The uterus may be ill defined because of inflammation.  Endometritis may result in central-endometrial-cavity echo thickening and heterogeneity  Hydrosalpinx is depicted as a fluid-filled fallopian tube – If the fallopian tube walls are thickened and if debris is present within the tube, pyosalpinx should be considered in the differential diagnosis.  Oophoritis results in enlarged ovaries with ill-defined margins that often appear adherent to the uterus; adjacent free fluid may be present in the adnexa or cul-de- sac.  TOAs are depicted as complex adnexal masses with thickened walls and central fluid. Imaging findings in TOAs must be distinguished from: Endometriomas, Ectopic pregnancies, Hemorrhagic cysts, Ovarian tumors, Abscesses from adjacent organs.  Pelvic infection, with findings of tubal inflammation and hydrosalpinx detected by Doppler studies, is one of the most specific criteria in diagnosing PID.
  23. 23. CT findings in PID may include the following: o In early PID are typically subtle, Often the only findings are fluid in the pouch of Douglas and pelvic fat inflammation. As the infection progresses, CT features of PID include fluid filled fallopian tubes with thick walls and enlarged ovaries with a heterogeneous or partly cystic appearance. A tubo-ovarian abscess represents a more advanced stage of PID. o CT findings of perihepatitis: capsular enhancement (due to increased blood flow) along the surface of the liver most commonly seen on the right-anterior hepatic surface. o Hepatomegaly, intra-parenchymal reversible dynamic perfusion abnormalities.
  24. 24. Investigations:  Laparoscopy(Gold standard) is indicated if the diagnosis is unclear or there is no response to treatment after 48 hours, Findings: hyperemia and edema of tubes, purulent exudates from fimbrial ends, tubes are not freely movable, pyosalpinx, violin string like adhesions in the pelvis and around the liver.  Culdocentesis: to rule out ectopic pregnancy and to establish diagnosis of pelvic abscess.  Investigations are also to be extended to male partner and smear and culture are made from urethral secretion. Hydrosalpinx on Ultrasound
  25. 25. anechoic tubular structures in adnexa; hydrosalpinx tubular structure with debris in left adnexa : pyosalpinx bilateral complex masses in patient who had pyometrium: tubo-ovarian abscess echogenic region within endometrium with dirty shadowing; finding is compatible with air in endometrium and endometritis
  26. 26. Hydrosalpinx on Ultrasound
  27. 27. Laparoscopy Findings of PID
  28. 28. Laparoscopy Findings of PID
  29. 29. Acute Salpingitis: edema, erythema, and exudate of the fallopian tube
  30. 30. Complications:  Tuboovarian abscesses and pelvic peritonitis, formation of adhesions, hydrosalpinx or pyosalpinx.  Dyspareunia.  Right upper quadrant pain associated with perihepatitis (Fitz-Hugh–Curtis syndrome) can occur and may be the dominant symptom.  In pregnancy, PID is uncommon but has been associated with an increase in both maternal and fetal morbidity.  Women with HIV may have more severe symptoms associated with PID.  Infertility rate is 12%, after two episodes increases to 25% and after three raises to 50%. It is due to tubal damage or tubo-ovarian mass.  Chronic pelvic inflammation is due to recurrent or associated pyogenic infection.  Increased risk of ectopic pregnancy.
  31. 31. Fitz-Hugh–Curtis syndrome:
  32. 32. Fitz-Hugh–Curtis syndrome:  Fitz-Hugh-Curtis syndrome(FHCS) was named after Thomas Fitz-Hugh and Arthur Hale Curtis in 1930 and in 1934 when they saw the purulent patch and “violin-string” like fibrous adhesions between the liver and anterior peritoneum or the diaphragm, also known as perihepatitis.  (FHCS) occurs in 4–27% of patients with PID. It is an acute perihepatitis caused by Chlamydia trachomatis or Neisseria gonorrhoeae, al-though 30%- 40% of cases are polymicrobial and thought to represent ascending infection from PID. Bacteria spread by means of direct extension along the right paracolic gutter or through the lymphatic system causing inflammation of the right upper quadrant peritoneal surfaces of the liver.  It poses a diagnostic challenge when presenting with isolated right upper quadrant abdominal pain, and without signs and symptoms of PID, as the symptoms of primary pelvic inflammation are either subtle or have resolved by the time of presentation.
  33. 33. Fitz-Hugh–Curtis syndrome:  (FHCS) can be misdiagnosed as it may present like many other disorders including pulmonary embolism, pneumonia, Cholecystitis, renal colic, and perforated ulcer.  A diagnostic gold standard for (FHCS) has not been established. Although laparoscopy has been suggested for definitive diagnosis of (FHCS) in the past, with the far less invasive multislice contrast-enhanced (CT) now widely available, it has become less frequently used, especially in emergency settings.  The management of (FHCS) is similar to that of PID. In addition, the lysis of the adhesion bands may be done laparoscopically for symptomatic relief. The long-term complications include abdominal pain, small bowel obstruction, and infertility.  (FHCS) should always be considered in women with infertility and the under surface of the liver should always be visualized during laparoscopy for tubal patency in all cases of infertility especially with background of PID.
  34. 34. Fitz-Hugh–Curtis syndrome
  35. 35. Violin String adhesions of Fitz-Hugh-Curtis Syndrome
  36. 36. lysis of the adhesion bands are performed laparoscopically
  37. 37. PID Treatments:  The choice of an appropriate treatment regimen may be influenced by:  local antimicrobial sensitivity patterns.  local epidemiology of specific infections in this setting.  Cost.  Patient preference and compliance.  severity of disease.  Most patients with PID are managed as outpatients, but hospitalization should be considered for patients with the following conditions:  Uncertain diagnosis.  Pelvic abscess on Ultrasonographic scanning, and confirmed by CT or MRI.  Surgical emergencies cannot be excluded.
  38. 38. PID Treatments:  Pregnancy.  Inability to tolerate outpatient oral antibiotic regimen.  Severe illness, severe nausea, vomiting, or a fever >38.5ºC.  Immunodeficiency.  Failure to improve clinically after 48/72 hours of outpatient therapy. It has to be noted that: • Delaying treatment increases the risk of long-term sequelae such as ectopic pregnancy, infertility and pelvic pain. • In inpatients, the treatment response can be monitored by changes in C-reactive protein and white cell count. • Intravenous therapy, when given, should be at least continued until 24 hrs after clinical improvement and then switched to oral. • Dosage recommendations may need to be adjusted depending on local licensing regulations and the availability of drug formulations. • The optimal duration of treatment is not known but most clinical trials report a response to 10–14 days of therapy.
  39. 39. PID Treatments: • Recommended regimens: 1- Outpatient regimens: A- Regimen: -oral ofloxacin 400 mg twice daily or levofloxacin 500 mg once daily + oral metronidazole 500 mg twice daily for 14 days.
  40. 40. PID Treatments: • 1- Outpatient regimens: • B- Regimen: • -I.M ceftriaxone 500 mg single dose, followed by oral doxycycline 100 mg twice daily + metronidazole 500 mg twice daily for 14 days  Metronidazole is included to improve coverage for anaerobic bacteria that may have a role in the pathogenesis of PID, however, it might be discontinued in patients with mild or moderate PID , or those who are unable to tolerate it.  Oral moxifloxacin 400 mg once daily for 14 in patients who are positive for M. genitalium.
  41. 41. PID Treatments: • OR: Cefoxitin 2 g IM once as a single dose concurrently with probenecid 1 g orally in a single dose, or ‎another single-dose parenteral third-generation cephalosporin (eg. cefotaxime)+ ‎ doxycycline 100 mg orally twice daily for 14 days.  Metronidazole 500 mg orally twice daily for 14 days can be added ‎if there is evidence or ‎suspicion of vaginitis or if the patient underwent gynecologic instrumentation in the preceding ‎‎2-3 weeks‎.
  42. 42. PID Treatments: • 2-Inpatient regimens: A- Regimen: Cefoxitin 2 g IV every 6 hours plus i.v. doxycycline 100 mg twice daily(oral doxycycline may be used if tolerated). This regimen is continued for 24 hours after the patient remains clinically improved, after which doxycycline 100 mg is given orally twice daily for a total of 14 days
  43. 43. PID Treatments / Inpatient regimens: 2-Inpatient regimens: B- Regimen: -Clindamycin 900 mg IV every 8 hours plus Gentamicin IV in a loading dose of 2 mg/kg, followed by a maintenance dosage of 1.5 mg/kg q8h. - IV therapy may be discontinued 24 hours after the patient improves clinically, and oral therapy with 100 mg doxycycline twice daily should be continued for a total of 14 days. -If TOA is present, clindamycin or metronidazole may be used with doxycycline for more effective anaerobic coverage. -If ceftriaxone is not readily available, cefixime 400 mg can be given orally in combination with either azithromycin or doxycycline. -if ceftriaxone cannot be given because of severe allergy, azithromycin 2 g can be given orally in a single dose.
  44. 44. PID Treatments :  The following Key Points should be taken into consideration:  Current partners of women with PID should be contacted and offered health advice and screening for gonorrhoeae and Chlamydia, and if diagnosed, should be treated appropriately.  Partners should be advised to avoid unprotected intercourse until they and their partner have completed the treatment course.  If tubo-ovarian abscess does not respond in (48–72 hours) to antimicrobial therapy, surgery (Colpotomy, Percutaneous drainage/aspiration, or Exploratory laparotomy) might be considered, also in cases of ruptured abscess.  The patient should be educated to avoid reinfection and the potential hazards of it,(warned against multiple sexual partners and to use condoms).  Follow-up: Review at 72 h is recommended. Failure to improve suggests the need for further investigation and management including repeating microbiology testing.  Repeating smears and cultures are to be done after 7 days following the full course of treatment and following each menstrual period until it becomes negative for three consecutive reports.
  45. 45. PID Treatments  The following Key Points should be taken into consideration:  While triad of lower abdominal pain, adnexal tenderness and tender cervical movements are considered to be the most important clinical features of Acute PID, chronic PID presents as chronic abdominal pain, congestive dysmenorrhea, deep dyspareunia, menstrual abnormalities and infertility, with signs of tenderness on one or both iliac fossa, an irregular tender pelvic mass, PR examination - Involvement of parametrium & uterosacral ligament.  In management of Chronic Pelvic Infection, Investigations, imaging & diagnostic procedures are similar to acute PID. Broad spectrum Antibiotics for 3 weeks/ based on culture sensitivity. Surgery is indicated in case of: -Persistence of symptoms despite conservative management. -Recurrence of acute attack. -Increase in size of pelvic mass despite treatment. -Persistent menorrhagia & deterioration in general health.

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