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INFLAMMATORY DISEASES OF THE FEMALE GENITALIA�

Днепропетровск

2016

КУ «Днепрпоетровская областная больница им. И.И. Мечникова»

кафедра акушерства и гинекологии ГУ «ДМА МЗ Украины»

АКУШЕР-ГИНЕКОЛОГ ВЫСШЕЙ КАТЕГОРИИ

Д.М.Н., ПРОФЕССОР

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CLASSIFICATION

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Facultative anaerobes

Obligatory anaerobes

Gram-positive cocci

Staphylococcus:

S. aureus

S. epidermidis

S. saprophyticus

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Streptococcus:

S. pyogenes

S. agalactiae

S. faecalis (Enterococcus)

Petrococcus

Petrostreptococcus

Gram-negative cocci

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Neisseria gonorrhoeae

Veillonela

S. aureus

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gonococcus

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CLASSIFICATION

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Facultative anaerobes

Obligatory anaerobes

Gram-negative rod-shaped bacteria

Eschericha coli

Citrobacter

Klebsiella: K. pneumoniae

K. oxitoca

Enterobacter: E. cloacae

E. aerogenes

Serratia marcescens

Proteus: P. vulgaris

P. mirabilis

Providencia: P. rettgeri

P. alcalifaciens

Gardnerella vaginalis

Pseudomonas

Bacteroides:

B. fragilis

B. bivium

B. oralis

B. melaninogenicus

Mobiluncus

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gardnerella

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the key cells

gardnerella

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CLASSIFICATION

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Facultative anaerobes

Obligatory anaerobes

Gram-positive rod-shaped bacteria

Listeria monocytogenes

Clostridium perfringens

Obligatory intracellular pathogens

Chlamydia trachomatis

Microorganisms without the cellular wall

Mycoplasma hominis

Ureaplasma urealyticum

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WAYS OF THE INFECTION SPREAD

  1. Intracanalicular transport

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  • Hematogenic way

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  • Lymphogenic way

trichomonas

Trichomonas vag.

spermatozoids

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FACTORS, WHICH FACILITATE THE DEVELOPMENT OF THE INFLAMMATION

  • Mechanical
  • Thermal
  • Chemical
  • Mental overstrain
  • Excessive physical load
  • Blood loss
  • Endocrine disturbances
  • Stress
  • Allergic factors
  • Change in the microflora of vagina

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FACTORS INFLUENCING COMPOSITION OF NORMAL VAGINAL MICROFLORA

  1. The pH of vaginal contents, which is connected with the function of ovaries.
  2. Physiological status of woman, which is changed in dependence on the age, menstrual cycle, during pregnancy and postpartum period.
  3. Sexual activity.
  4. Use of contraceptives.
  5. Different diseases.
  6. Application of antibiotics.
  7. Reduction in the local and general immunity.

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PATHOGENESIS OF INFLAMMATION

Pathologic

Clinical

  1. Alteration

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  • Stage of the vascular disorders

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  • Stage of the proliferation
  1. Alterative inflammation or the stage of the infiltration (dystrophia and necrosis)

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  • The exudative inflammation (it is characterized by the expressed disturbance of blood circulation with the phenomena of exudation)

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  • The proliferating or productive inflammation (it is characterized by the development of connective tissue - by scar regeneration)

damage, tissue change

the osmotic pressure is reduced

degree of colloid dispersion rises

the normal relationship of the electrolytes

(increased [K]+ and lowered Ca+) is disrupted

Tissue acidosis

Disorders in tissue metabolism

edema

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CLASSIFICATION

  1. According to the form of the agent
    1. Nonspecific – staphylococcus, streptococcus, Escherichia coli, anaerobic bacteria et al.
    2. Specific – mycobacterium tuberculoses, gonococcus, trichomonas vaginalis, mycoplasma hominis and others
    3. Viruses – HSV, VHP
    4. Fungi
    5. Protozoa

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  • According to the exudates
    • serous
    • serous-bloody
    • serous-purulent
    • purulent

HPV

herpes simplex virus

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CLASSIFICATION

  1. Course:
    1. Acute
    2. Subacute
    3. Chronic
      • Primary chronic process
      • Chronic relapse
      • Residual state of chronic.

For specific process

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  1. Fresh process (up to two months)
    1. acute
    2. subacute
    3. torpid
  2. Chronic – when the disease has continued for over two months or when its onset is unknown.
  3. Latent form (presence of the agent in the absence of clinical signs)

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CLASSIFICATION

  1. By localization:
    1. Inflammation of external genitalia –

vulvitis, bartolinitis, vaginitis

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2. Inflammation of internal genitalia – endocervicitis, endometritis, myometritis, salpingitis, oophoritis, peritonitis.

candidosis

Candida albicans on

vaginal wall

vulvitis ( in girl 10-years as a result

of insufficient hygiene)

vulvovaginitis in the 5 yo girl

pointed condylomas

in the 2 yo girl

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STAGES

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Cervicitis

Endometritis

Salpingitis

Oophoritis

Tubo-ovarian abscess

Peritonitis

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DIAGNOSTICS OF THE INFLAMMATORY DISEASES

  1. Anamnesis
  2. Complaints

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    • pain
    • the burning
    • pain during the urination
    • the itch, which leads to insomnia and to the disorder of nervous system, amplifying during mensis

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Characteristic for the inflammatory diseases of external sex organs

    • increase in body temperature
    • quickening of the pulse
    • chills
    • uterine hemorrhage
    • the severe pains of below stomach with the irradiation in inguinal region, the region of sacrum, sheath, rectum (irradiation depends on the localization inflammatory center)
    • the dysuric phenomena

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Characteristic for the inflammatory diseases of the internal sex organs

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DIAGNOSTICS OF THE INFLAMMATORY DISEASES

  1. Laboratory methods (bacteriological, bacterioscopic)
  2. Endoscopic (сolposkopya, gysteroskopya, diagnostic)

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  • Immunological

hysteroscopy

immunological test

laporoscopy

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DIAGNOSTICS OF TUBERCULOSIS OF THE SEX ORGANS

  1. Laparoscopy
  2. Diagnostic curetage with histological and microbiological study

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  • Aspiration biopsy of the menstrual blood with its subsequent culture (not less than 3times during one menses). Possibly bacterioscopic and bacteriological study cervical secret.
  • X-ray examination of lungs, gastrointestinal tract, urinary tracts

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  • Urine culture for mycobacterium of tuberculosis

D&C

biopsy of endometrium

hysterosalpingography

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ENDOMETRITIS

Endometritis – inflammation of the mucous membrane of the uterine body. Rarely it may be isolated, the most often the muscular layer of the uterus is also involved (metroendometritis).

Risck factors:

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      • Abrasio cavi uteri
      • Complications during labours
      • Intrauterine manipulations

Clinic:

      • Pain in the lower abdomen, which irradiates to the loin and thighs, malaise, fever, high temperature, leycocytosis.

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The acute phase of inflammation lasts about five days. The mucous membrane of endometrium sloughs away with possibility of self-healing. More frequently endometritis progresses to endomyometritis and perimetritis with risk of septic condition.

Acute endometritis

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PARAMETRITIS

  1. Parametritis – inflammation of the parauterine cellular tissue. Anterior, posterior and lateral parametritis are distinguished.

involvement in the infectious process

of the pelvic peritoneum

Exudation

in the

recto-uterine pouch

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PID : DEFINITION

  • 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
  • Sexually transmitted organisms, especially N. gonorrhoea and C. trachomatis, are implicated in many cases
  • However, microorganisms that comprise the vaginal flora (e.g., anaerobes, G. virginals, Haemophilus influenzae, enteric Gram-negative rods, and Streptococcus agalactiae) also have been associated with PID
  • In addition, M. [Mycoplasma] hominis and U. [Ureaplasma] urealyticum might be etiological agents of PID

Center for Disease Control & Prevention (CDC)

Treatment Guidelines 2010

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PID

  1. Salpingo-oophoritis - inflamation of a uterine tube and the associated ovary.

Edema and damage of tissues lead to obstruction of the lumen of the tube with the accumulation of exudate

and formation of

      • hydrosalpinx
      • pyosalpinx
      • haematosalpinx

pyosalpinx

adnexitis

adhesions

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PID RISK FACTORS

PID commonly occurs in women < 35. It is rare before menarche, after menopause, and during pregnancy.

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Risk factors include

  • Previous PID
  • Presence of bacterial vaginosis or any sexually transmitted disease

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Other risk factors, particularly for gonorrheal or chlamydial PID, include

  • Younger age
  • Nonwhite race
  • Low socioeconomic status
  • Multiple or new sex partners

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PID : EPIDEMIOLOGY

Risk factors

ACCEPTED

PROPOSED

1. Menstruating teens

1. Low socio-economic status

2. Multiple sex partners

2. Early age of sexual activity

3. Prior H/O PID

3. Urban living

4. Sexually Transmitted Infection

4. High frequency of coitus

5. Non-use of barrier contraceptive

5. Use of IUCD

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6. Cigarette smoking

7. Substance abuse

8. Douching

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PID : EPIDEMIOLOGY

Protective

  1. Barrier methods: Specially condom with spermicidal chemicals (Nonoxynol-9 which is bactericidal & virucidal)
  2. Oral steroidal contraceptives: -Thick mucus plug (preventing ascend of sperm and bacterial penetration) -Decrease in duration of menstruation (Short interval of bacterial colonization of the upper tract)
  3. Women with monogamous partner with vasectomy
  4. Pregnancy
  5. Menopause
  6. Uncommon in women who are not menstruating
  7. Husband who is azoospermic

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PID : MICROBIOLOGY

  • Acute PID: Usually polymicrobial

Primary organisms

  • Sexually transmitted

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Secondary organisms

  • Normally found in vagina

Aerobic: Non-hemolytic streptococcus, E. coli,

Group-B streptococcus & staphylococcus

Anaerobic: Bacteroides species- fragilis & bivius, Peptostrepococcus & peptococcus

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PID : MODE OF TRANSMISSION

Ascending infection (Canalicular spread)

  • Ascend of gonococcal & chlamydial organisms by surface extension from the lower genital tract through the cervical canal by way of the endometrium to the fallopian tubes
  • Facilitated by the sexually transmitted vectors such as sperms & trichomonads

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  • Reflux of menstrual blood along with gonococci into the fallopian tubes may be the other possibility

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PID : MODE OF TRANSMISSION

Gynecological procedures favoring ascend of infection

  • E.g. D&C, D&E

Blood-borne transmission

  • Pelvic tuberculosis

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Direct spread from contaminated structures in abdominal cavity

  • E.g. Appendicitis, cholecystitis

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ACUTE PID : PRESENTATION & DIAGNOSIS

  • Diagnosis of Acute PID is difficult because of wide variation & non-specific nature of symptoms & signs
  • Many women with PID have subtle or mild symptoms

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  • A diagnosis of PID usually is based on clinical findings
  • Delay in diagnosis and treatment probably contributes to inflammatory sequelae in the upper reproductive tract

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ACUTE PID : PRESENTATION & DIAGNOSIS

History

  • The patient should be asked about the location, intensity, radiation, timing, duration, and exacerbating and mitigating factors of the pelvic pain: Bilateral lower abdominal & pelvic dull aching pain is characteristic of acute PID
  • H/O Fever (Oral temperature > 38.3˚C/101F)
  • H/O Abnormal vaginal discharge
  • H/O symptoms suggestive of dysuria
  • Previous H/O abdominal or gynecological surgeries
  • H/O previous gynecological problem
  • H/O IUD insertion (6 times higher risk within 20 days)
  • Social history: Should include patient’s sexual and STDs history & partner’s history in terms of STDs

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ACUTE PID : PRESENTATION & DIAGNOSIS

Fitz Hugh & Curtis Syndrome

  • Consists of rt. upper quadrant pain resulting from ascending pelvic infection and inflammation of the liver capsule or diaphragm
  • Although it is typically associated with acute salpingitis, it can exist without signs of acute pelvic inflammatory disease (PID)

Physical examination

  • Abdominal & pelvic examination is most important
  • Bilateral abdominal tenderness
  • Adnexal mass & adnexal tenderness
  • Cervical motion tenderness
  • Uterine tenderness
  • Vaginal mucopurulent discharge

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ACUTE PID : MOST COMMON DD

Most common DD of acute PID

1. Appendicitis

2. Ectopic pregnancy

3. Endometritis

4. Ovarian cyst

5. Ovarian torsion

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ACUTE PID : DIFFERENTIAL DIAGNOSIS

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ACUTE PID : DIFFERENTIAL DIAGNOSIS

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ACUTE PID : CDC DIAGNOSIS CRITERIA

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ACUTE PID : STAGING

(I-IDSOG-USA recommends following stages)

Stage I

  • Women who fulfil the CDC major diagnostic criteria and >1 of its minor criteria but who do not have overt peritonitis (as demonstrated by the absence of rebound tenderness) and who have not had any prior documented STD upper tract infections

Stage II

  • The above criteria, with peritonitis

Stage III

  • Women with demonstrable tubo-ovarian complex or tubo-ovarian abscess evident on either physical or ultrasonographic examination

Stage IV

  • Women with ruptured tubo-ovarian abscesses

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PELVIC PERITONITIS

��Pelvic peritonitis – is an inflammation of the pelvic peritoneum developing as a complication of inflammatory process in the pelvic organs (salpingo ophoritis, pyovarum, necrosis of leyomatous node). �

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PELVIC PERITONITIS

Clinical picture:

  • Sharp abdominal pain
  • High pyrexia
  • Tachycardia
  • Nausea
  • Vomiting
  • Abdominal distension, tension of the abdominal wall, tenderness, positive Blumberg symptom.
  • Bimanual examination shows bulking of posterior fornix, its tenderness with palpation, and tenderness with cervical displacement.

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KEY POINTS ABOUT PID

  • The sexually transmitted pathogens Neisseria gonorrhoeae and Chlamydia trachomatis are common causes of PID, but infection is often polymicrobial.
  • PID can cause tubal scarring and adhesions, which commonly result in chronic pelvic pain, infertility, and increased risk of ectopic pregnancy.
  • Because even minimally symptomatic infection may have severe sequelae, index of suspicion should be high.
  • PCR and cultures are accurate tests; however, if results are not available at the point of care, empiric treatment is usually recommended.
  • Hospitalize women with PID based on clinical criteria (see above).

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ТREATMENT OF THE INFLAMMATORY DISEASES

Organism

Antibiotics

N. gonorrhea

Cephalosporins, Quinolones

Chlamydia

Doxycycline, Erythromycin & Quinolones (Not to cephalosporins)

Anaerobic organisms

Flagyl, Clindamycin &

in some cases to Doxycycline

ß-Haemolytic streptococci.

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E. coli

Penicillin derivatives, Tetracyclines, and Cephalosporins.,

E. Coli is most often treated with the penicillins or gentamicin

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MANAGEMENT : PARENTERAL

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  • Because of the pain associated with intravenous infusion, doxycycline should be administered orally when possible
  • Oral and IV administration of doxycycline provide similar bioavailability
  • Parenteral therapy can be discontinued 24 hours after clinical improvement, but oral therapy with doxycycline (100 mg twice a day) should continue to complete 14 days of therapy
  • When tubo-ovarian abscess is present, clindamycin or metronidazole with doxycycline can be used for continued therapy rather than doxycycline alone because this regimen provides more effective anaerobic coverage

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CDC-2010 Regimen A

Cefotetan 2 g IV every 12 hours

or

Cefoxitin 2 g IV every 6 hours

PLUS

Doxycycline 100 mg orally or IV every 12 hours

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MANAGEMENT : PARENTERAL

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  • Parenteral therapy can be discontinued 24 hours after clinical improvement
  • On-going oral therapy should consist of doxycycline 100 mg orally twice a day, or clindamycin 450 mg orally four times a day to complete a total of 14 days of therapy
  • When tubo-ovarian abscess is present, clindamycin should be continued rather than doxycycline, because clindamycin provides more effective anaerobic coverage

CDC-2010 Regimen B

Clindamycin 900 mg IV every 8 hours

PLUS

Gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours

  • Single daily dosing (3–5 mg/kg) can be substituted

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MANAGEMENT & FOLLOW-UP

Out-patient

Oral regimen

In-patient

Parenteral regimen

3 Days (72 hours)

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Substantial clinical improvement ????

  • Defervescence
  • Reduction in direct or rebound abdominal tenderness
  • Reduction in uterine, adnexal & cervical motion tenderness

NO

  • Reassessment of patient & treatment
  • Additional diagnostic testing

After 6 - months

Repeat testing of all women who have been diagnosed with chlamydia or gonorrhoea

Yes

  • Switch to oral from parenteral after 24 hours of clinical improvement
  • If on oral – continue the same

Admit Out-patient

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PID : CHRONIC COMPLICATIONS & SEQUELAE

Complications

1. Dyspareunia

2. Infertility : due to tubal factor

  • 12 % after single episode
  • 25 % after two episodes
  • 50 % after three episodes

3. Increased risk of ectopic pregnancy

  • 6-10 % increase in risk following H/O PID

4. Formation of adhesion or hydrosalpinx or pyosalpinx & tubo -ovarian abscess

5. Chronic pelvic inflammation

  • Due to recurrent or associated pyogenic infection/ T.B.

6. Chronic pelvic pain and ill health

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Thank you for your attention!

моб.: +38 (067) 737-81-17

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http://medvedev.ua

Днепропетровск

2016

АКУШЕР-ГИНЕКОЛОГ ВЫСШЕЙ КАТЕГОРИИ

Д.М.Н., ПРОФЕССОР