Pelvic Inflammatory Disease

1. PID
“Pelvic inflammatory disease”
By/ Asmaa Ghanem
Fourth year medical student at FOM-PSU.

2. Definition
Etiology
Types
 Acute PID
 Chronic PID

3. Definition
PID is a clinical spectrum of infection that may involve one
or more or the following structures: (7)
The cervix (cervicitis), the endometrium (endometritis), the
fallopian tube (salpingitis), the ovary (oophoritis), the uterine
wall (myometritis), the uterine serosa and broad ligaments
(parametritis), and the pelvic peritonium (peritonitis).
Infection & Inflammation of the upper genital tract i.e.
Tubes, ovaries, pelvic peritonium (+/- uterus) 2-3% of
population.
 Types
Acute last 2-3 days Chronic

4. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Chronic PID

5. ChronicAcute
1) Sequelae of acute PID
(inadequate TTT / neglected cases)
2) Chronic from the start
Polymicrobial infection
Caused by
1. STDs
2. Non-specific
3. Chronic granulomatous ( TB )
1. Primary :
STDs (sexually transmitted)
Chlamydia trichomatis (60%),
Neisseria gonorrhoeae (40%)
2. Secondary : non-specific
(normally found in vagina)
I. Aerobic
II. Anaerobic
(Mixed)
 Etiology
 Organism
 Predisposing factors
 Routes of infection

7. 2 STDs
Gyna
2 Obst
Must open to
pass the organism
1. Mucous mem &cilium
2. Wall
3. Peritonium (except)

8. Etiology
 Organism
 Predisposing factors
 Sexually active females with multiple sexual partners
(usually after menses “loss of cx plug, degenerated endometrium,
retrograde menstruation”)
 IUCD users (Barriers + COC PID)
 Recent instrumentation of uterus (D&C /HSG )
 Routes of infection
 Ascending “Endogenous” through:
Lumen endosalpingitis
Lymphatics interstitial salpingitis
 Direct neighboring organs perisalpingitis
 Blood “Hematogenous” T.B. endo-, interstitial,
peri- salpingitis

9. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Etiology
 Pathology
 Clinical picture
 DD
 Investigations
 Complications
 TTT
 Chronic PID

10. Etiology:
1. STD's Chlamydia trichomatis (60%), Neisseria gonorrhoeae (40%)
2. Puerperal or post-abortive
3. Non-specific organisms (aerobic or anaerobic): usually mixed
Pathology:
a) Acute catarrhal salpingitis
- Resistance: high
- Infection only of m.m. serous exudate in lumen
- Fate complete resolution
b) Acute suppurative salpingitis
- Virulence: high
- Infection (Pus) to all layers purulent exudate in lumen
- Fate chronicity, spread (pelvic peritonitis)
c) Acute perisalpingitis fimbrial adhesions closure of
fimbrial end.
If Obstruction: Partial ectopic, Total infertility
1- resistance of host
2- virulence of organism

11. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Etiology
 Pathology
 Clinical picture
 Investigations
 Complications
 DD
 TTT
 Chronic PID

12. congestive symptoms : (according to site)
1- Pain
Vagina: dyspareunia
Uterus: dysmenorrhea
Rectum: dyschezia (painful defecation)
Bladder: dysuria
Back: dorsal pain
Abdomen : deep aching abdominal pain
2- Bleeding
Uterus: menorrhagia
Ovary: poly menorrhea
3- Discharge
Odorless : (non-infected) Leucorrhea
Offensive : infection, pus, purulent, mucopulurent
Investigations
1- Organism: C & S
Culture+smear Ag detection Serology
2- Organ: C B C
Culture Blood See (U/S, Laproscopy)

13. Clinical picture
1) Symptoms (history of PDF +)
• General FAHM-R
• Abdominal acute lower abdominal pain
• Pelvic congestive symptoms (pain, bleeding, discharge)
2) Sings
• General signs of infection (pulse, Tm, look toxic)
• Abdominal tenderness & rigidity in lower abdomen (peritonitis)*
maximum 3 cm above mid-inguinal point (tubal point)
• P/V tender movement of cx, tender adenexae +/- tender mass
Bimanual ex (T only no mass), Speculum ex (discharge).
ALL SYMPTOMS ARE NON-SPECIFIC

14. Investigations:
Culture: swab from 1ry &2ndry sites (Chlamydia invade single layer columnar cells)
endocervix, Bartholin G, Skene’s Gland, rectum, pharynx.
Blood: ESR, TLC, CRP
differentiate Acute from Chronic
Complications: (see the infection)
 U/S: TOA “Tubo-ovarian abscess”, Adnexal swelling. DD
*Teratoma *Ectopic pregnancy *inflammatory
 Laparoscopy: GOLD STANDARD
red, swollen, edematous tube (+/- mass)
pus may exudate from fimbrial end cytology
Criteria for diagnosis

15. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Etiology
 Pathology
 Clinical picture
 Investigations
 Complications
 DD
 TTT
 Chronic PID

16. Complications
1- Chronicity, recurrence (deep racemose gland of cervix,
antibiotic does not reach it).
2- Obstruction: of tubes leads to Infeftility, Ectopic
pregnancy
3- Spread: “septic focus”
- Pelvic abscess formation
- Thrombophlebitis
- Peritonitis
- Septicemia

17. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Etiology
 Pathology
 Clinical picture
 Investigations
 Complications
 DD
 TTT
 Chronic PID

18. Treatment
 Prophylaxis 1- Avoid SIDs 2- Aseptic techniques 3- Early diagnosis
 Active
1- General lines .. If diffuse inflammation NOT localizes & abscess.
(Antipyretics, Analgesics, Antibiotic), rest “Fowler”, partner TTT
2-Antibiotic therapy: in combination (continued 48 hrs after resolution of
fever)
o Regimen I.......cefoxitin (2nd) or cefotaxime (3rd) + Doxycycline
o Regimen II... .. .clindamycin + gentamycin
o Regimen III...ampicillin + gentamycin + metronidazole (triple antibiotic)
3- Hospitalization:
- Nulliparity or low pariry to avoid infertility
- Bad general condition (*large mass :TO mass, *complicated mass: ruptured)
4- Surgical intervention: If
* Severe, medical ttt failed * ruptured /huge TOA*generalized peritonitis
Laparotomy + drainage + peritoneal toilet
(+/- Unilateral adenxectomy), Pelvic clearacne (TAH+ BSO)
*If small tuboovarian abscess aspiration (U/S guided or Laparoscopy)
*Pelvic abscess drain by posterior colpotomy
*Thrombophlebitis heparin
5- TTT of specific organism:

19. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Chronic PID
 Etiology
 Pathology
 Clinical picture
 DD
 Investigations
 TTT

20. Pathology: (5)
1) Hydrosalpinx: Acute catarrhal salpingitis
* Serous fluid, thin wall, mild adhesions + pelvic pressure & pain.
* More: torsion, infection, rupture. HSG = retort shaped swelling
2) Hydrosalpinx + Inflammatory ovarian cyst = Tubo-ovarian cyst
3) Pyosalpinx: Acute suppurative salpingitis
* Thickened tube, full of pus, dense adhesions
* Less torsion. HSG = smaller in size
4) Pyosalpinx + ovarian abscess = Tubo-ovarian abscess
5) Perisalpingitis : Acute perisalpingitis
6) Salpingitis isthmica nodosa (chronic interstitial salpingitis)
* Thickened, interstitial abscess, Obstruction
Multiple bilateral nodules & diverticula (esp in isthmus)
7) Fitz-Hugh-Curtis syndrome
* Perihepatitis associated with chronic PID.
C/P recurrent upper right abdominal pain.
Inv. laparoscopy violin string-like bands of adhesions.

22. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Chronic PID
 Etiology
 Pathology
 Clinical picture
 DD
 Investigations
 TTT

23. Clinical picture
1) History: previous attacks of acute PID or ectopic
2) Symptoms
o Infertility
o congestive symptoms
o Recurrent acute exacerbations
3) Sings
General: ill health TB toxemia.
Abdominal: sings of TB peritonitis or bilharziasis HSM
Pelvic: *tenderness (Lower abdominal, cervical motion)
* TO (adenxal) mass *Fixed RVF
DD: Endometriosis, cancer ovary, TB

24. Definition
Etiology
 Organism
 Predisposing factors
 Routes of infection
Types
 Acute PID
 Chronic PID
 Etiology
 Pathology
 Clinical picture
 DD
 Investigations
 TTT

26. Definition
Etiology
Types
 Acute PID
 Chronic PID
 Pelvic abscess