PID and TOA Management by residents at Level Two Teaching hospital

We send this presentation for academic purpose

1. David, OBGYN specialist
KabgayiL2TH,Rwanda

2. Contents
Definition
Epidemiology
Pathophysiology
Etiology
Risk factors
Classification
Clinical presentation
differentials
Management
Tuboovarianabscess
Complications and management

3. Definition
Infection of upper female reproductive tract
Spectrum disease involve cx, uterus, tubes
Most often ascending spread of
microorganisms from vagina & endocervixto
endometrium, tubes, contiguous structures
Incidence acute PID 1-2% of young sexually
active women each year
Lead to infertility , ectopic, Abcess,chronic
pelvic pain,adhesions

4. Epidemiology
PID occurs most frequently in women ages 15 to 25
years.
In 2001 there were more than 750,000 cases of PID in
the United States
CDC has estimated that more than 1 million women
experience an episode of PID every year
PID in africaremain undiagnosed, estimated to 900,000
yearly cases.
the prevalence of STI syndromes amongst individuals
screened at health facilities in Rwandavaried between
2.37% to 4.16%

6. Pathophysiology
Most often , ascending spread of microorganisms
from vagina & endrocervixto endometrium, tubes,
contiguous structures

8. Etiology
Neisseriagonorrhoeaecommon cause of PID
85% of infection sexually active female of
reproductive age
15% of infection occur after procedures that
break cervical mucous barrier
Bacteria culture direct from tubal fluid common :
N. gonorrhoeae, C. trachomatis, Trichomonas
vaginalis,endogenous aerobic, anaerobic, genital
mycoplasmaspp.

9. Risk factors

10. Risk factors cont’
Strong correlation between exposure to STD
Age of 1
st
intercourse
Frequency of intercourse
Number of sexual partners
Marital status; 33% in nulliparous
Increase risk
IUD user (multifilament string)
Surgical procedure
Previous acute PID
Reinfectionif untreated male partner (80%)

11. Classifications
Acute PID
Chronic PID
PID complicated to TOA

12. Clinical presentation
Common clinical manifestation
lower abdominal pain 90%
cervical motion tenderness
adnexaltenderness/uterine tenderness
Fever above 38.3.
Mucopulrulentcervical discharge
leukocytosis

14. Differential diagnosis
acute appendicitis
Endometriosis
torsion/rupture adxmass
ectopic preg
lower genital tract infection

15. Management
Admission for IV treatment

16. Management cont’
Acute PID; treatment as IV in inpatient
Chronic PID treatment as outpatient/ depending on
clinical presentation (Rwandan Protocol)

17. IV treatment
Ceftriaxone/ Doxy/ metronidazoleiv

18. OPD treatment for mild symptoms
Oral

19. Tuboovarianabscess (TOA)
With the ascending infection in genital reproductive
tract, with neigboringpelvic organs lead to
salpingitis,oophoritis, peritonitis, perihepatitis,and
TOA
TOA:Agglutination/collection of pus as complication
of PID, may involve bowel and bladder,
It is serious, life threatening condition
Rare association with pregnancy

20. TOA cont’
Aggressive medical or surgical management is
required, is rupture, results sepsis, mortality 50%
Incidence of TOA is increasing, from 14-40years
Multiple sexual paterners, prior PID,HIV infection

21. Pathophysiology
Ascending inflammation/damage of
endometrium/destroy secretory/cilliarytube
mechanism,odema, then blockage,Ischemia, necrosis,
pyoslapinx.Untreated,
Pus collection/complex mass/cavities for microbes to
grow/anaerobsthen sepsis

22. Microbiology
Polymicrobial
Mixatureof aerobics and anaerobs
E coli, streptococcus,bactroidesfragilis, prevotella
anaerobs; peptostreptococcus.
Candida species
Rarely TB
Rarely Neisseriagonorrhea, chlamydia
trachomatis/ though to facilitate invasion than being
causative of TOA

23. Presentation
Abdominal pain.fever,chills,vaginadischarge
Fever not present in all patients
In 175 Cases: 40% afebrile, 25% chronic rather
than acute pain.
Most of patients not in overt septic.
If ruptured: signs of sepsis and acute abdomen.

24. Diagnosis
I.History / examination , background of PID
II.Lab test: CBC, ESR,CRP,cervicaltest/swab for
gonorrhe/ chlamydia, pregnancy test
III.Imaging test:Ultrasound, CT scan
IV.Laparoscopy
V.No response to antibiotics last 48hr-72hrs
u/s decription: assess Douglas. Free fluids,
complexemultilocularmass, with oblitarated
adenexalanatomy, contain fluids, internal echoes

25. U/S findings

26. Differentials
ovarian mass/ ovarian torsion, ruotureovarian cyst,
PID, degenertivefibroids, dysmenorrhea,septic
abortion.
Ectopic pregnancy
Appendicitis/ appenducularabcess
Pyeronephritis.,cystitis,nephrolithiasis

27. Medical Management
Medical treatment Candidates
Hemodynamicallystable, no sign of rupture/sepsis
Small abscess less than 7cm , responds well to ATB
Premenopausal
Adequate response to ATB
Clinical improvement on ATB

28. Antibiotherapy

30. Management cont’
Other regimen
Ampiccilin+Clinidamycin+Gentamycin
Levofloxaccin+metronidazole
Imipenem+cilastatin

31. Management cont’
Require in patient observation 48-72hrs due to
serisousrisk of rupture and sepsis
Daily WBC count monitoring response to ATB
Every 3days U/S to assess size of the mass showing
response if decreasing
Duration of ATB 14days minimum by CDC
When drained duration 10-14days

32. Management cont’
Oral treatment as outpatient if
Afebrilefor 48-72hrs,nromal wbc,improvingabdminal
tenderness
Toralateoral medications
Able to comply with communication/follow up
Metronidazole+doxy
Clindamycin+doxy
Lovofloxaccin+metronidazole
Azithromyicin+metronidazole
Amoxiccillin–clavulanate2gr twice perday

33. Management cont’
Failed medical management
48-72hrs on iv atbno response
New onset of fever/ persistence
Persistence/worsening abdominal tenderness
Enlarging pelvic mass
Suspected sepsis
Persistent/worsening leukocytosis
High CRP
Consider surgical management/drainage!

34. Surgical management
Surgical evaluation is indicated
In case of abscess rupture/sepsis
Postmenopausal patients/ association with
malignancy 2.5-40%
Abscess of 7cm or greater
Failed medical mgt for 48-72hrs

35. Surgical pproach
Explorative laparotomy/ Drainage ;Fluids/ pus sent
to lab for culture and sensitivity
Laparoscopy if not rupture
Experienced surgeon/challenges;distorted
anatomy,friabletissues risk for bowel injuries
Remove much abcesscavity,aspiratefluids,
pus,Irrigatethe cavity, lessening all infectious side
Combine with ATB after surgery

36. Surgical approach cont’
Given high rate of ssidue contamination by cavity
abscess, it is recommended
Close fascia with monofilament non absobableor
delayed absorbable suture
Leave skin and subcutanousopen for at least 72hrs
Wound can be healed by delayed closure
procedure or by secondary intension
Many surgeon prefer primary skin closure
Suction drain my be usefulltill the patient improve or
discharge minimal.

37. Complications+management
Adhesions and chronic pelvic pain 4x higher
Tubal damage 10%
Infertility 20%
•Ectopic pregnancy increases 6-10 fold
Pelviperitonitis
Perihepatitis﴾Fitz-Hugh-Curtis syndrome ﴿1-10%
perihepaticinflammation & adhesion
s/s ; RUQ pain, pleuriticpain, tenderness at RUQ on
palpation of the liver
mistaken dx; acute cholecystitis, pneumonia
Death 1%
Prevention; condoms, limited role for contraception,

38. Complications cont’

39. References
Uptodate.com/ PID, TOA
https://www.cdc.gov/std/treatment-
guidelines/pid.h
Williams Gynecology P 66-70
Pelvic Inflammatory Disease: Diagnosis,
Management, and Prevention Amy Curry, MD et al
OBS-GYN Rwandan Protocole

40. Thank you