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GENITAL TRACT INFECTIONS AND
PELVIC INFLAMMATORY DISEASE
Julius M. Kwedhi
6th year, Medical Faculty, Sechenov University
Gynaecology Class
(29 November 2018)
Differential Diagnoses
• A 35 years old female, gravida
2, para 2, presents with a
history of severe midline lower
abdominal pain that started 2
days ago. Her menses started
at age 13.
• Question: What are the
differential diagnoses of acute
and chronic lower abdominal
pain?
Answers
• Endometriosis
• Ovarian cysts accident (torsion,
haemorrhage, rupture)
• Appendicitis
• Cystitis
• Diverticulitis
• Ectopic Pregnancy
• Tumors
• Trapped Ovarian Syndrome
• Mittelschmerz
• Primary Dysmenorrhea
• Pelvic Inflammatory Disease
• Ischemic Bowel Disease
• Inflammatory Bowel Disease
• Irritable Bowl Syndrome
• Intestinal Obstruction (Volvulus,
Intussusception etc)
• Strangulated Hernia
• Salpingoorphoritis
• Adnexitis
• Peritonitis
• Vulvovaginitis
• Adenomyosis
• UTI
• Renal/Bladder Calculi
PART 1
• GENITAL TRACT INFECTION
Normal Vaginal Flora
• Normally, 5 to 15 different bacterial species (both
aerobic and anaerobic):
• Lactobacillus acidophilus
• group B streptococcus,
• Escherichia coli,
• Prevotella
• Etc.
Infection of the Vulva and Vagina
1.Non-sexually Transmitted Infections
2.Sexually Transmitted Infections
Non-sexually Transmitted
Infections
• Candidiasis
• Bacterial vaginosis (formerly known as Gardnerella
or anaerobic vaginosis)
• Infection from foreign bodies (TSS)
Sexually Transmitted Infections
• Chlamydia (C. Trachomatis)
• Gonorrhoea (N. Gonorrhoea)
• Genital Warts (Condylomata Acuminata - HPV)
• Genital Herpes (HSV 2)
• Syphilis (T. Pallidum)
• Trichomoniasis (T. Vaginalis)
• Human Immunodeficiency Virus
Vulvovaginitis
Etiology Symptoms Clincal Signs Diagnostic Method
Monilial vaginitis Pruritus
Thick white discharge;
pH 4.0–4.7
Wet mount prep or
KOH prep
(pseudohyphae)
Trichomonas
Malodorous discharge,
pruritus
Frothy, copious yellow-
green discharge; pH 5-
7
Wet mount prep (motile
trichomonads)
Bacterial vaginosis Discahrge, fishy odor
Thin, gray discharge;
pH 5-5.5
Wet mount prep, sniff
test (clue cells)
Chlamydia Discharge
Mucopurulent
discharge, cervical
erosion
Culture; MicroTrak or
Chlamydiazyme
Gonorrhea Discharge Cervical discharge
Cervical culture; gram
stain
Genital herpes Pain
Ulcerative, vulvar
vesicles & ulcers
Virus culture, Tzank
prep
Chemical Discharge
Erythema; may be
ulcerative
History & exclusion of
other causes
PART 2
• PELVIC INFLAMMATORY DISEASE
Introduction
• Pelvic inflammatory disease (PID) comprises a
spectrum of inflammatory diseases of the upper
genital tract of women. PID can involve infection
of the endometrium (endometritis), the oviducts
(salpingitis), the ovaries (oophoritis), the uterine
wall (myometritis), or portions of the parietal
peritoneum (peritonitis).
• PID is usually the result of a sexually transmitted
disease (STI) and less often results from
iatrogenic causes after instrumentation of the
female reproductive tract.
Definitions
• Acute PID refers to the acute symptoms accompanying
ascending infection from the cervix to the endometrium,
tubes, ovaries, and pelvic peritoneum.
• Chronic PID refers to chronic pelvic pain, often periodic in
exacerbation, which can follow an acute episode of PID, a
sequelae to the infl ammatory response to an acute infection
in the pelvis. Chronic pelvic infection can also be caused by
the more rare pelvic infection with tuberculosis (TB) and
actinomycosis.
• Silent PID refers to asymptomatic or mildly symptomatic
pelvic infection, which is usually diagnosed when the
sequelae of tubal damage is found at a later date.
Medical Sequelae
• Develop in one in four women with acute PID:
• Tubal obstruction that leads to infertility
• Ectopic pregnancy rate increases 6 to 10 fold
• Chronic pelvic pain in 20%
• Mortality as a result of ruptured tuboovarian
abscess that leads to septic shock and death
Risk Factors
• Frequent sexual activity
• Early onset of sexual activity
• Multiple sex partners
• Recent new sex partner
• Intrauterine devices (IUD
Prophylaxis
• Male & female condoms
• Oral contraceptives
• decrease menstrual flow,
• decrease ability of pathogenic bacteria to attache to
endometrial cells
• Progestin-induced changes in the cervical mucus that
retard the entrance of bacteria.
• Other barrier methods of contraception (e.g. the
diaphragm, sponge, contraceptive foam)
Bacteriology
• Acute PID is usually a polymicrobial infection caused by
normal flora of the cervix and vagina:
• Neisseria gonorrhoea (cervix & fallopian tubes)
• Chlamydia Trachomatis (cervix & fallopian tubes)
• Polymicrobial uterus and fallopian tubes infection by:
• Escherichia coli, Gardnerella vaginalis,Streptococcus
species, Proteus, Klebsiella, and Haemophilus
influenzae, Bacteroides, Peptostreptococcus, and
Peptococcus
• Actinomyces israelii (IUD-associated, unilateral
abscesses)
Pathophysiology
• When PID occurs, salpingo-oophoritis is usually preceded by cervical infection with gonorrhea and/or
chlamydia; infection ascends when an inciting event occurs that allows bacteria to ascend into the
uterus and then into the tubal lumen, usually bilaterally. Symptomatic ascending infection follows
10% to 40% of cervical infections with gonorrhea and chlamydia.
• Inciting Events:
1. Menstrual periods
2. Sexual intercourse
3. Bacterial vaginosis (BV) - Gardnerella vaginalis & Mycoplasma organisms
4. Iatrogenic events:
1.Elective abortion
2.Dilation and curettage and endometrial biopsy
3.IUD insertion or use
4.Hysterosalpingography
5.Chromopertubation at laparoscopy
Chronology of Salpingo-
oorphoritis
• Infection is usually bilateral, but unilateral infection is also possible,
especially in association with an IUD. The clinical course is as follows:
• Endosalpingitis develops initially with edema and ultimately proceeds to
destruction of luminal cells, cilia, and mucosal folds. Bacterial toxins are
most likely to be responsible.
• Infection spreads to the tubal muscularis and serosa. It also spreads by
direct extension to the abdominal cavity through the fi mbriated end of the
tube.
• Oophoritis develops over the surface of the ovaries, and microabscesses
may develop within the ovaries.
• Peritonitis may occur, and upper abdominal infection may result either by
direct extension of infection up the abdominal gutters laterally or by
lymphatic spread. Development of perihepatitis with adhesions and right
upper quadrant abdominal pain is known as Fitz–Hugh–Curtis syndrome.
Sequelae of PID
• a. Pyosalpinges (tubal abscesses)
• b. Hydrosalpinges (fl uid-fi lled, dilated, thin-walled, destroyed tubes,
usually totally obstructed)
• c. Partial tubal obstruction and crypt formation
• d. Total tubal obstruction and infertility
• e. Tubo-ovarian abscesses
• f. Peritubal and ovarian adhesions
• g. Dense pelvic and abdominal adhesions
• h. Ruptured abscesses, resulting in sepsis and shock
• i. Chronic pelvic pain and dyspareunia
Minimum Diagnostic Criteria
• a. Lower abdominal tenderness
• b. Uterine or adnexal tenderness
• c. Cervical motion tenderness: lateral motion of
the cervix on examination causes pain by putting
tension on the adnexa
Additional Diagnostic Criteria
• For women with severe signs, these additional criteria are used to increase the specificity
of the diagnosis:
• a. Oral temperature higher than 100.9 ° F (38.3 ° C) present in less than one-third of
women diagnosed with PID
• b. Abnormal cervical or vaginal discharge. Mucopurulent cervical discharge with white
blood cells (WBCs) seen on wet mount is almost always seen in women with PID. If this
finding is not present, other diagnoses should be seriously entertained
• c. Elevated erythrocyte sedimentation rate (ESR)
• d. Elevated C-reactive protein
• e. Positive test for gonorrhea or chlamydia
• f. Tubo-ovarian abscess seen on ultrasound
• g. Evidence of endometritis on endometrial biopsy
• h. Laparoscopic evidence of PID
Diagnosis
• 3. Other symptoms that may be seen in women
with PID include
• a. Abdominal pain
• b. Intermenstrual and/or postcoital bleeding
• c. Urinary frequency
• d. Nausea/vomiting
• e. Lower back pain
Differential Diagnosis
• 1. Ectopic pregnancy
• 2. Ruptured ovarian cyst
• 3. Appendicitis
• 4. Endometriosis
• 5. Inflammatory bowel disease
• 6. Degenerating fi broids
• 7. Spontaneous abortion
• 8. Diverticulitis
Diagnostic Techniques
• Cervical gram stain
• Serum Beta hCG
• Ultrasound
• CT Scan
• Laparoscopy
• Blood studies
• Leukocytosis is not a reliable indicator of acute PID
• ESR, although nonspecific, it is, nevertheless, elevated in 75% of laparoscopically
confirmed cases
• Follow up (48-72 hrs)
• Test for HIV and Pap smear creating
Treatment
• Individualized treatment
• Oral treatment regimens:
• Ceftriaxone 250 mg IM,
• Cefoxitin2 g IM with probenecid 1g orally at the
time of injection or other 3rd gen.
cephalosporin,
• Doxycycline 100 mg oral bd for 14 days,
• Metronidazole 500 mg bd for 15 days
Treatment
• Parenteral regimens:
• Regimen A:
• Cefotetan 2g IV every 12 hrs, or cefoxitin
2g IV every 6 hrs
• Plus Doxycycline 100 mg PO or IV every
12 hrs. Oral Clindamycin or metronidazole
may be added if abscess is suspected
Treatment
• Regimen B
• Clindamycin 900 mg IV every 8hrs +
Gentamicin 2mg/kg loading dose IV or IM
followed by 1.5 mg/kg maintenance dose
every 8 hrs
• When conversion to oral therapy takes place:
Doxycycline 100 mg bd or clindamycin 450
mg qd

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Genital Tract Infections - Dr. Julius King Kwedhi

  • 1. GENITAL TRACT INFECTIONS AND PELVIC INFLAMMATORY DISEASE Julius M. Kwedhi 6th year, Medical Faculty, Sechenov University Gynaecology Class (29 November 2018)
  • 2. Differential Diagnoses • A 35 years old female, gravida 2, para 2, presents with a history of severe midline lower abdominal pain that started 2 days ago. Her menses started at age 13. • Question: What are the differential diagnoses of acute and chronic lower abdominal pain?
  • 3. Answers • Endometriosis • Ovarian cysts accident (torsion, haemorrhage, rupture) • Appendicitis • Cystitis • Diverticulitis • Ectopic Pregnancy • Tumors • Trapped Ovarian Syndrome • Mittelschmerz • Primary Dysmenorrhea • Pelvic Inflammatory Disease • Ischemic Bowel Disease • Inflammatory Bowel Disease • Irritable Bowl Syndrome • Intestinal Obstruction (Volvulus, Intussusception etc) • Strangulated Hernia • Salpingoorphoritis • Adnexitis • Peritonitis • Vulvovaginitis • Adenomyosis • UTI • Renal/Bladder Calculi
  • 4. PART 1 • GENITAL TRACT INFECTION
  • 5. Normal Vaginal Flora • Normally, 5 to 15 different bacterial species (both aerobic and anaerobic): • Lactobacillus acidophilus • group B streptococcus, • Escherichia coli, • Prevotella • Etc.
  • 6. Infection of the Vulva and Vagina 1.Non-sexually Transmitted Infections 2.Sexually Transmitted Infections
  • 7. Non-sexually Transmitted Infections • Candidiasis • Bacterial vaginosis (formerly known as Gardnerella or anaerobic vaginosis) • Infection from foreign bodies (TSS)
  • 8. Sexually Transmitted Infections • Chlamydia (C. Trachomatis) • Gonorrhoea (N. Gonorrhoea) • Genital Warts (Condylomata Acuminata - HPV) • Genital Herpes (HSV 2) • Syphilis (T. Pallidum) • Trichomoniasis (T. Vaginalis) • Human Immunodeficiency Virus
  • 9. Vulvovaginitis Etiology Symptoms Clincal Signs Diagnostic Method Monilial vaginitis Pruritus Thick white discharge; pH 4.0–4.7 Wet mount prep or KOH prep (pseudohyphae) Trichomonas Malodorous discharge, pruritus Frothy, copious yellow- green discharge; pH 5- 7 Wet mount prep (motile trichomonads) Bacterial vaginosis Discahrge, fishy odor Thin, gray discharge; pH 5-5.5 Wet mount prep, sniff test (clue cells) Chlamydia Discharge Mucopurulent discharge, cervical erosion Culture; MicroTrak or Chlamydiazyme Gonorrhea Discharge Cervical discharge Cervical culture; gram stain Genital herpes Pain Ulcerative, vulvar vesicles & ulcers Virus culture, Tzank prep Chemical Discharge Erythema; may be ulcerative History & exclusion of other causes
  • 10. PART 2 • PELVIC INFLAMMATORY DISEASE
  • 11. Introduction • Pelvic inflammatory disease (PID) comprises a spectrum of inflammatory diseases of the upper genital tract of women. PID can involve infection of the endometrium (endometritis), the oviducts (salpingitis), the ovaries (oophoritis), the uterine wall (myometritis), or portions of the parietal peritoneum (peritonitis). • PID is usually the result of a sexually transmitted disease (STI) and less often results from iatrogenic causes after instrumentation of the female reproductive tract.
  • 12. Definitions • Acute PID refers to the acute symptoms accompanying ascending infection from the cervix to the endometrium, tubes, ovaries, and pelvic peritoneum. • Chronic PID refers to chronic pelvic pain, often periodic in exacerbation, which can follow an acute episode of PID, a sequelae to the infl ammatory response to an acute infection in the pelvis. Chronic pelvic infection can also be caused by the more rare pelvic infection with tuberculosis (TB) and actinomycosis. • Silent PID refers to asymptomatic or mildly symptomatic pelvic infection, which is usually diagnosed when the sequelae of tubal damage is found at a later date.
  • 13. Medical Sequelae • Develop in one in four women with acute PID: • Tubal obstruction that leads to infertility • Ectopic pregnancy rate increases 6 to 10 fold • Chronic pelvic pain in 20% • Mortality as a result of ruptured tuboovarian abscess that leads to septic shock and death
  • 14. Risk Factors • Frequent sexual activity • Early onset of sexual activity • Multiple sex partners • Recent new sex partner • Intrauterine devices (IUD
  • 15. Prophylaxis • Male & female condoms • Oral contraceptives • decrease menstrual flow, • decrease ability of pathogenic bacteria to attache to endometrial cells • Progestin-induced changes in the cervical mucus that retard the entrance of bacteria. • Other barrier methods of contraception (e.g. the diaphragm, sponge, contraceptive foam)
  • 16. Bacteriology • Acute PID is usually a polymicrobial infection caused by normal flora of the cervix and vagina: • Neisseria gonorrhoea (cervix & fallopian tubes) • Chlamydia Trachomatis (cervix & fallopian tubes) • Polymicrobial uterus and fallopian tubes infection by: • Escherichia coli, Gardnerella vaginalis,Streptococcus species, Proteus, Klebsiella, and Haemophilus influenzae, Bacteroides, Peptostreptococcus, and Peptococcus • Actinomyces israelii (IUD-associated, unilateral abscesses)
  • 17. Pathophysiology • When PID occurs, salpingo-oophoritis is usually preceded by cervical infection with gonorrhea and/or chlamydia; infection ascends when an inciting event occurs that allows bacteria to ascend into the uterus and then into the tubal lumen, usually bilaterally. Symptomatic ascending infection follows 10% to 40% of cervical infections with gonorrhea and chlamydia. • Inciting Events: 1. Menstrual periods 2. Sexual intercourse 3. Bacterial vaginosis (BV) - Gardnerella vaginalis & Mycoplasma organisms 4. Iatrogenic events: 1.Elective abortion 2.Dilation and curettage and endometrial biopsy 3.IUD insertion or use 4.Hysterosalpingography 5.Chromopertubation at laparoscopy
  • 18. Chronology of Salpingo- oorphoritis • Infection is usually bilateral, but unilateral infection is also possible, especially in association with an IUD. The clinical course is as follows: • Endosalpingitis develops initially with edema and ultimately proceeds to destruction of luminal cells, cilia, and mucosal folds. Bacterial toxins are most likely to be responsible. • Infection spreads to the tubal muscularis and serosa. It also spreads by direct extension to the abdominal cavity through the fi mbriated end of the tube. • Oophoritis develops over the surface of the ovaries, and microabscesses may develop within the ovaries. • Peritonitis may occur, and upper abdominal infection may result either by direct extension of infection up the abdominal gutters laterally or by lymphatic spread. Development of perihepatitis with adhesions and right upper quadrant abdominal pain is known as Fitz–Hugh–Curtis syndrome.
  • 19. Sequelae of PID • a. Pyosalpinges (tubal abscesses) • b. Hydrosalpinges (fl uid-fi lled, dilated, thin-walled, destroyed tubes, usually totally obstructed) • c. Partial tubal obstruction and crypt formation • d. Total tubal obstruction and infertility • e. Tubo-ovarian abscesses • f. Peritubal and ovarian adhesions • g. Dense pelvic and abdominal adhesions • h. Ruptured abscesses, resulting in sepsis and shock • i. Chronic pelvic pain and dyspareunia
  • 20. Minimum Diagnostic Criteria • a. Lower abdominal tenderness • b. Uterine or adnexal tenderness • c. Cervical motion tenderness: lateral motion of the cervix on examination causes pain by putting tension on the adnexa
  • 21. Additional Diagnostic Criteria • For women with severe signs, these additional criteria are used to increase the specificity of the diagnosis: • a. Oral temperature higher than 100.9 ° F (38.3 ° C) present in less than one-third of women diagnosed with PID • b. Abnormal cervical or vaginal discharge. Mucopurulent cervical discharge with white blood cells (WBCs) seen on wet mount is almost always seen in women with PID. If this finding is not present, other diagnoses should be seriously entertained • c. Elevated erythrocyte sedimentation rate (ESR) • d. Elevated C-reactive protein • e. Positive test for gonorrhea or chlamydia • f. Tubo-ovarian abscess seen on ultrasound • g. Evidence of endometritis on endometrial biopsy • h. Laparoscopic evidence of PID
  • 22. Diagnosis • 3. Other symptoms that may be seen in women with PID include • a. Abdominal pain • b. Intermenstrual and/or postcoital bleeding • c. Urinary frequency • d. Nausea/vomiting • e. Lower back pain
  • 23. Differential Diagnosis • 1. Ectopic pregnancy • 2. Ruptured ovarian cyst • 3. Appendicitis • 4. Endometriosis • 5. Inflammatory bowel disease • 6. Degenerating fi broids • 7. Spontaneous abortion • 8. Diverticulitis
  • 24. Diagnostic Techniques • Cervical gram stain • Serum Beta hCG • Ultrasound • CT Scan • Laparoscopy • Blood studies • Leukocytosis is not a reliable indicator of acute PID • ESR, although nonspecific, it is, nevertheless, elevated in 75% of laparoscopically confirmed cases • Follow up (48-72 hrs) • Test for HIV and Pap smear creating
  • 25. Treatment • Individualized treatment • Oral treatment regimens: • Ceftriaxone 250 mg IM, • Cefoxitin2 g IM with probenecid 1g orally at the time of injection or other 3rd gen. cephalosporin, • Doxycycline 100 mg oral bd for 14 days, • Metronidazole 500 mg bd for 15 days
  • 26. Treatment • Parenteral regimens: • Regimen A: • Cefotetan 2g IV every 12 hrs, or cefoxitin 2g IV every 6 hrs • Plus Doxycycline 100 mg PO or IV every 12 hrs. Oral Clindamycin or metronidazole may be added if abscess is suspected
  • 27. Treatment • Regimen B • Clindamycin 900 mg IV every 8hrs + Gentamicin 2mg/kg loading dose IV or IM followed by 1.5 mg/kg maintenance dose every 8 hrs • When conversion to oral therapy takes place: Doxycycline 100 mg bd or clindamycin 450 mg qd