GYN 11

• Genital tract defense


  Free anastomosis between lymphatics and blood vessels, direct communication of peritoneal cavity to exterior through vagina
• Vulvar defense


  • Anatomic: Apposition of cleft by labia, Compound racemose type of Bartholin's glands
  • Physiologic: Fungicidal action of secretion, Natural high resistance to infection of vulvar and perineal skin
• Vaginal defense

  • Anatomic: Apposition of anterior and posterior walls with transverse rugae, Stratified epithelium devoid of glands
  • Physiologic: Maintained by estrogen
• Vaginal defense at birth

  Maternal estrogen circulating into newborn, Vaginal epithelium becomes multilayered, Desquamated epithelium containing glycogen converted into lactic acid by Lactobacillus acidophilus
• Vaginal defense after birth till puberty


  No circulatory estrogen, Vaginal epithelium reduced to few layers, Glycogen absent, Doderlein's bacillus absent, Vaginal pH neutral or alkaline
• Vaginal defense during reproductive period

  High estrogen, Vaginal defense fully restored
• Vaginal defense after menopause

  Estrogen deficiency, Lack of glycogen in vaginal epithelial cells, Vaginal pH rises, Lactic acid production less
• Only Doderlein's bacilli can grow in acidic media with pH 4-4.5, When pH increases other organisms will grow
• Phases of life when vaginal defense is lost


  • Following 10 days of birth till puberty
  • During menstruation
  • Following abortion and childbirth
  • During menopause
• Cervical defense


  • Anatomic: Racemose type of glands, Mucus plug
  • Physiologic: Bactericidal effect of mucus
• Uterine defense


  • Cyclic shedding of endometrium, Closure of uterine ostium of fallopian tube with inflammatory reaction
• Tubal defense

  • Anatomic: Integrated mucus plicae and epithelial cilia
  • Physiologic: Peristalsis and cilia movement towards uterus
• Causative organisms of upper genital tract infections

  • Pyogenic (50%): Aerobes (Staphylococcus, Lactobacillus, Diphtheroids, E. coli, Pseudomonas, Klebsiella, N. gonorrhoeae), Anaerobes (Anaerobic streptococcus, Clostridium, Peptostreptococcus, Bacteroides)
  • Sexually transmitted disease (STD): N. gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, Herpes simplex virus type II, Human papilloma virus, Gardnerella vaginalis, Haemophilus ducreyi, Donovan bodies, HIV, Mycoplasma
  • Parasitic: Trichomonas vaginalis
  • Fungal: Candida albicans
  • Viral: Herpes simplex virus type II, Human papillomavirus, HIV, Condylomata accuminata
  • Tubercular: Mycobacterium tuberculosis
• Modes of spread of infections


  • Through continuity and contiguity - gonococcal infection
  • Through lymphatics and pelvic veins - postabortal and puerperal infection
  • Through bloodstream - tubercular
  • From adjacent infected extragenital organs like intestine
• Causes of acute pelvic infection

  • Pelvic inflammatory disease (PID)
  • Following delivery and abortion
  • Following gynecological procedures
  • Following intrauterine devices (IUD)
  • Secondary to other infections - appendicitis
• Pelvic inflammatory disease (PID)


  Spectrum of infection and inflammation of the upper genital tract organs typically involving the uterus, fallopian tubes, ovaries, pelvic peritoneum and surrounding structures, Attributed to ascending spread of microorganisms from cervicovaginal canal
• Terminology used to express specific organ pathology: endometritis, salpingitis, pelvic peritonitis, tubo-ovarian abscess, parametritis. Cervicitis not included.
• Epidemiology of PID


  • Incidence 1-2% per year among sexually active women, 85% spontaneous infection in sexually active females, 15% following procedures, Two-thirds in young women <25 years, One-third in 30 years or older
• Changes in epidemiology of PID

  • Shift from inpatient to outpatient PID
  • Change in clinical presentation - less severe disease commonly seen
  • Shift in microbial etiology - more Chlamydia trachomatis than gonococcus
• Risk factors for PID

  • Sexually active teenagers
  • Younger age (<19 years)
  • Multiple sexual partners
  • Absence of contraceptive pill use
  • Previous history of acute PID
  • IUD users (not with LNG-IUS)
  • Lower socioeconomic status
  • Husband/sexual partner with urethritis or STI
  • Genetic predisposition
• Protective factors against PID

  • Barrier methods, especially condom, diaphragm with spermicides
  • Oral steroidal contraceptives - thick mucus plug, shorter menstruation interval
  • Monogamy or partner with vasectomy
  • Pregnancy
  • Menopause
  • Vaccines: Hepatitis B, HPV
  • Postcoital washing (urethra, genital skin)
• Primary organisms in acute PID

  • N. gonorrhoeae (30%)
  • Chlamydia trachomatis (30%)
  • Mycoplasma hominis (10%)
• Secondary organisms in acute PID

  • Aerobic: Nonhemolytic streptococcus, E. coli, Group B streptococcus, Staphylococcus
  • Anaerobic: Bacteroides species, Peptostreptococcus, Peptococcus
• Modes of affection in acute PID

  • Gonococcus ascends through mucosal continuity and contiguity, facilitated by sexually transmitted vectors
  • Reflux of menstrual blood with gonococci into fallopian tubes
  • Mycoplasma hominis spreads across parametrium to affect tube
  • Secondary organisms affect tube through lymphatics
  • Rarely, organisms from gut may affect tube directly
• Pathology of acute PID

  • Bilateral involvement of tubes, Destruction of epithelial cells, cilia and microvilli, Invasion of all tubal layers, Edema and hyperemia, Closure of tubal ostia, Formation of hydrosalpinx or pyosalpinx, Pelvic peritonitis and tubo-ovarian abscess
• Symptoms of acute PID

  • Bilateral lower abdominal and pelvic pain
  • Fever, lassitude and headache
  • Irregular and excessive vaginal bleeding
  • Abnormal vaginal discharge
  • Nausea and vomiting
  • Dyspareunia
  • Pain and discomfort in right hypochondrium (Fitz-Hugh-Curtis syndrome)
• Fever >38°C, Bilateral lower abdominal tenderness, Cervical motion tenderness, Adnexal tenderness are clinical features of acute PID
• Abscess


  A localized collection of pus within the tissues of the body
• Symptoms of acute PID

  • Bilateral lower abdominal and pelvic pain
  • Fever, lassitude and headache
  • Irregular and excessive vaginal bleeding
  • Abnormal vaginal discharge
  • Nausea and vomiting
  • Dyspareunia
  • Pain and discomfort in the right hypochondrium
• Clinical features of acute PID

  • Fever >38°C
  • Bilateral lower abdominal tenderness with radiation to the legs
  • Abnormal vaginal discharge
  • Abnormal uterine bleeding
  • Deep dyspareunia
  • Cervical motion tenderness
  • Adnexal tenderness/mass
• Laparoscopic examination in acute PID

  • Inflamed liver capsule with classic violin string adhesions to the parietal peritoneum and beneath the diaphragm
• Signs of acute PID

  • Temperature elevated to beyond 38.3°C
  • Abdominal palpation reveals tenderness on both the quadrants of lower abdomen
  • Vaginal examination reveals abnormal vaginal discharge, congested external urethral meatus, congested cervix with purulent discharge, bilateral tenderness on fornix palpation
• Minimum criteria for diagnosing acute PID (CDC - 2015)

  • Lower abdominal tenderness
  • Adnexal tenderness
  • Cervical motion tenderness
• Additional criteria for diagnosing PID (CDC - 2015)

  • Oral temperature >38°C
  • Mucopurulent cervical or vaginal discharge
  • Abundant WBCs on saline microscopy of cervical secretions
  • Raised C-reactive protein
  • Elevated ESR
  • Laboratory documentation of positive cervical infection with Gonorrhea or C. trachomatis
• Definitive criteria for diagnosing PID (CDC - 2015)

  • Histopathologic evidence of endometritis on biopsy
  • Imaging study (TVS/MRI) showing evidence of thickened fluid filled tubes, ± free pelvic fluid or tubo-ovarian complex
  • Laparoscopic evidence of PID
• Identification of organisms in PID

  1. Collect discharge from urethra, Bartholin's gland, cervical canal

  2. Perform Gram stain and culture (aerobic and anaerobic)
• Gram-negative diplococci


  Suggestive of gonococcal infection
• Detection of C. trachomatis is difficult, so treatment should be started from the clinical diagnosis
• Leukocyte count


  Shows leukocytosis to more than 10,000 per cu mm
• ESR


  Elevated value of more than 15 mm per hour, correlates with severity of inflammatory reactions