Pelvic inflammatory disease is ascending infection from the endocervix. There are two main groups of organisms involved. These are STIs and commensals of the female genital tract
PID Basics - Causes, Symptoms and Treatment of Pelvic Inflammatory Disease
1. Pelvic Inflammatory
Disease - Basics
Indunil Piyadigama
54th Anuual Scientific Congress
Sri Lanka College of Obstetricians and Gynaecologists â 28th November 2021
2. PID
⢠Commonly used to describe
ascending pelvic infection from the
endocervix
⢠Involving at least the endometrium
and fallopian tubes
⢠A dynamic disease process involving
a variety of microorganisms
⢠Microorganisms that ascend from
the lower genital tract cause most
cases
⢠Less commonly, direct spread from
intra abdominal sepsis
⢠Usually associated with the bowel
⢠Rarely from blood-borne infection
such as tuberculosis
3. Aeitiology
⢠Two major groups of microorganisms associated with the disease
⢠Sexually transmitted infections(STIs)
⢠The endogenous flora of the lower genital tract
⢠Neisseria gonorrhea
⢠Chlamydia Trachomatous
⢠Genital mycoplasmas
⢠Endogenous anaerobes â Bacteroides, Prevotella, Gardnerella vaginalis,
Peptostreptococci species, Escherichia coli, Haemophilis influenzae
⢠Endogenous Aerobes - Streptococci
⢠Viral pathogens do not seem to have a role in the causation of PID
4. Swedish study 1970 to 1994
⢠Incidence of PID increased to a peak of 17.5 per 1000 women in the mid-
1970s
⢠75% of cases in women aged 15 to 24 were associated with chlamydial or
gonococcal infection in these studies
⢠Subsequently PID cases decreased to less than one per 1000 women in
1990 - 1994
⢠This correlated with
⢠IUD prescription to young nulliparous women in the mid-1970s
⢠Paralleled the decrease nationwide in gonorrhoea after 1975
⢠The introduction of successful programmes to control genital chlamydial infection
⢠Only minor changes in PID incidence occurred in women aged 30 or above
during the same period
5. Pathophysiology
⢠Younger women tend to have PID with Chlamydia and Gonorrhoea
⢠Older women tend to have PID more with endogenous vaginal organisms.
Therefore tend to have more suppurative disease
⢠Only a Small proportion of women with chlamydial or gonococcal cervicitis
develops upper genital tract infections
⢠No clear variation in virulence identified between different serotypes of these
pathogens
⢠Intermittent ascent of microorganisms may be a physiological occurrence
⢠Spermatozoa have been demonstrated to carry bacteria in to the pelvic cavity
⢠Dynamic process
⢠Begins as a mono microbial process initiated by primary pathogens such as N.gonorrhoeae
and C.trachomatis
⢠Progresses to become polymicrobial through the recruitment of endogenous bacteria
6. Pathophysiology continued
⢠Irreversible tubal deciliation
⢠Intraluminal adhesions and tubal occlusion can develop within days of the
onset of inflammation
⢠Direct effects of the pathogen
⢠The immune response (delayed type hypersensitivity)
⢠Delay in seeking care for more than a few days after the onset of pain is
associated with
⢠Significant increase in infertility
⢠Ectopic pregnancy
⢠Formation of a tubo-ovarian abscess is a late stage in the process of PID
when anaerobic bacteria predominate
7. Risk factors
⢠Chlamydial or gonococcal infection in the lower genital tract
⢠Demographic risk markers associated with sexual behaviour
⢠Young age (15-24)
⢠Being single, separated or divorced
⢠Low socioeconomic status
⢠Bacterial vaginosis
⢠Surgical instrumentation through the uterine cervix
⢠Termination of pregnancy
⢠IUD insertion â First six weeks after insertion. Risk decreases over the post insertion period
⢠Uterine evacuation
⢠Hysterosalpingography
⢠Vaginal douching
9. Clinical features of PID
⢠Can be symptomatic or asymptomatic
⢠The severity of tubal pathology in PID seems unrelated to the presence or
absence of a symptomatic episode
⢠Cardinal symptom is bilateral lower abdominal pain
⢠Cardinal clinical signs are bilateral adnexal tenderness and cervical excitation
⢠Abnormal vaginal discharge (50 - 60%)
⢠Irregular vaginal bleeding (35%)
⢠Dysuria (20%)
⢠Deep dyspareunia
⢠Systemic manifestations, including nausea, vomiting, malaise and temperature
⢠Considered severe PID if Fever > 380C, tubo-ovarian abscess formation, peritonitis
10. Fitz Hugh Curtis syndrome
⢠Cause right upper quadrant pain and right
hypochondrial tenderness
⢠Inflammation of the liver capsule with fibrinous
adhesions between the liver capsule and the
parietal peritoneum under the ribs is seen at
laparoscopy
⢠Up to 15% of patients with acute PID
⢠Due to perihepatitis from intraabdominal spread of
N. gonorrhoeae and C. trachomatis
11. Investigations
⢠Pregnancy test
⢠HIV testing
⢠Lower genital tract swabs, Endocervical swabs
⢠Positive gonorrhea or chlamydia in lower genital tract swabs supports
diagnosis
⢠Endocervical or vaginal pus cells
⢠Presence is nonspecific
⢠Only 20% positive predictive value for diagnosing PID
⢠But if pus cells negative highly unlikely to be having PID (95% NPV)
⢠ESR and CRP increase supports the diagnosis. But not specific
12. Laparoscopy
⢠Regarded as the definitive
investigation to diagnose PID
⢠The sensitivity of laparoscopy in
identifying salpingitis has been
reported as being as low as 50% when
compared with fimbrial histological
criteria
⢠Highlights the poor specificity of
clinical criteria
⢠Less than 10% of laparoscopically
confirmed salpingitis is unilateral
13. Management
⢠There are no definitive diagnostic criteria
⢠But PID can lead to severe consequences
⢠Therefore, low threshold should be maintained for treatment
⢠Adnexal tenderness in the absence of other diagnoses should be
regarded as the minimal criterion for the diagnosis of PID
⢠Incorrectly telling a patient that she has PID when she does not can
have psychological and social consequences
14. The aims of treatment
Alleviate the pain
and systemic
symptoms
associated with
infection
01
Achieve
microbiological
cure
02
Preserve fallopian
tube structure and
function
03
Prevent the spread
of infection to
others
04
16. Gonorrhoea
⢠50% women are asymptomatic
⢠Vaginal discharge
⢠Pain
⢠Urethritis
⢠These symptoms are found in
descending order of frequency
17. Diagnosis
⢠Nucleic acid amplification test (NAAT)
⢠Vaginal or cervical swabs can be used â Sensitivity 96%
⢠Urine is not sensitive in women
⢠Confirmation is with culture in Thyar Martin agar
⢠Endocervical or urethral swabs are used for culture
⢠Refrigerate the sample if delay in transport
⢠PCR can also be done on endocervical swabs
18. Management
Antibiotics
⢠IM Ceftriaxone 500mg single dose
or Oral Cefixime 400mg single dose
⢠IM Spectinomycin 2g single dose
Follow up
⢠Test of cure is recommended after
2 weeks due to emerging antibiotic
resistance
19. Chlamydia
⢠Clinical features
⢠80% of women are asymptomatic
⢠Diagnosis
⢠NAAT
⢠Sensitivity 95% with vulvovaginal
swabs
⢠Urine less sensitive
⢠SL â PCR from endocervical swabs
or urine
20. Management
⢠Oral Azithromycin 1g single dose
⢠Oral Doxycycline 100mg bd for 7 days
⢠Oral Erythromycin 500mg qds for 7 days
or Oral Erythromycin 500mg bd for 14
days
Antibiotics
⢠Not needed in Chlamydia
⢠If done for any reason recommended
after 6 weeks of treatment
Test of cure
21. Oral antibiotics for
PID
1. IM Ceftriaxone 500mg stat followed by Oral Doxycycline
100mg bd + Oral Metronidazole 400mg bd for 14 days
2. Oral Ofloxacin 400mg bd + Oral Metronidazole 400mg bd for
14 days
⢠Alternatively Levofloxacin 500mg daily can be used as an
alternative to Ofloxacin
⢠Regimes with metronidazole are useful in more symptomatic
where anaerobic coverage is needed
3. IM Ceftriaxone 500mg followed by Azithromycin 1g/week for 2
weeks
⢠This regime is preferred if suspecting gonorrhea as the
causative organism, since gonorrhea is getting resistant to
quinolones and cephalosporines
22. IV antibiotics for PID
1. IV Ceftriaxone 2g daily + IV Doxycycline 100mg bd
2. IV Clindamycin 900mg tds + IV Gentamycin 2mg/kg
dose followed by 1.5mg/kg tds
⢠IV antibiotics are preferred for severe PID
⢠Continue as in patient treatment till 24 hours of patient
becoming well
⢠Convert to oral antibiotics for 14 days
⢠HIV infected individuals have more severe symptoms.
But responds well to antibiotics
23. Surgical management
⢠In the minority of cases that do not
respond to conservative management
⢠Laparoscopy or laparotomy for
adhesiolysis and draining pelvic abscess
⢠Perihepatic adhesiolysis
⢠Ultrasound guided abscess drainage is
also equally effective
24. Treatment of the male partner
⢠Oral Azithromycin 1g stat
⢠Avoid intercourse until both partners have completed the treatment
course
⢠Barrier methods of contraception prevent PID
⢠Need to screen sexual contacts to prevent reinfection
25. Others
⢠Remove IUD and additional contraceptives for the given period
⢠IUD removal is usually recommended if the PID is severe enough to
warrant hospitalisation
⢠20% of patients with PID have recurrent attacks and an IUD might not
be the most appropriate contraceptive method
26. Follow up
⢠72 hours â for clinical improvement
⢠2-4 weeks
⢠To check for clinical response
⢠Compliance
⢠Sexual contact screening and treatment
⢠Repeat of pregnancy test
⢠Repeat testing for Chlamydia and gonorrhea at 6 weeks
⢠If continuing to have symptoms
⢠Poor compliance
⢠Sexual contacts positive for STI
⢠Positive pregnancy test
27. Complications
⢠Repeated pelvic infections lead to exponential increase in
complications
⢠Tubal factor infertility
⢠The risk of TFI after one episode of PID is about 8%
⢠Increasing to about 20% after two episodes
⢠To about 40% after three episodes or more
⢠Chronic pelvic pain has been reported in15-20%
⢠the first pregnancy after PID was ectopic in 9.1% of women compared
with 1.4% in the control women
28. Prevention
Primary prevention - measures to prevent exposure to infection
⢠Use of barrier methods
⢠Delaying the onset of sexual activity and exploring attitudes and values related to intercourse
⢠Most women with lower genital tract chlamydial or gonococcal infection are symptom free. Therefore
screening programs
⢠Treating cervical infections prior to uterine instrumentation
⢠RCOG - Patients undergoing termination of pregnancy should
⢠Either receive antibiotic prophylaxis or
⢠Screened for lower genital tract organisms with treatment of positive cases
⢠Non-pregnant patients under the age of 35 under going uterine instrumentation (for example IUD insertion)
should similarly be screened prior to the procedure or, failing that, should receive prophylactic antibiotics.
Secondary prevention - the detection and treatment of lower genital tract infection to prevent ascent to the
upper genital tract
Tertiary prevention - Early effective treatment to limit tubal damage
29. Conclusions
⢠PID is mainly a disease of the younger women
⢠PID can have a huge impact on future fertility
⢠STIs and endogenous organisms are the cuasative agents
⢠Difficult to diagnose since there is no specific criteria
⢠Important to have a low threshold for treatment
⢠There are many steps in preventing PID and its complications
30. References
⢠Sample collection manual for STI and HIV testing. National reference laboratory for STI and HIV. National STD/ AIDS control
programme in Sri Lanka
⢠Evidence based medicine
⢠Haitham Hamoda; Chris Bignell (2002). Pelvic infections. , 12(4), 0â190.doi:10.1054/cuog.2001.0258
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⢠Westr ̨mLetal.Pelvicin£ammatorydiseaseandinfertility.Acohort studyof1844womenwithlaparoscopicallyveri¢eddiseaseand 657
control women with normal laparoscopic ¢ndings. Sex Trans Dis1992; 185:185^192.
⢠Ross JDC. European guideline for the management of pelvic in£amma- tory disease and perihepatitis. Int J STD AIDS 2001;
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⢠MannS,SmithJR.Cervicitisandpelvicin£ammatorydisease.TheYear- book of Obstetrics and Gynaecology, Vol. 6. London: RCOG Press,
1998.
⢠Munday PE. Pelvic in£ammatory disease F an evidenced-based ap- proach to diagnosis. J Infect 2000; 40: 31^ 41.
⢠Eschenbach DA, Wolner-Hanssen P, Hawes SE, Pavletic A, Paavonen J, HolmesK.Acutepelvicin£ammatorydisease:associationsofclin-
icalandlaboratory¢ndingswithlaparoscopic¢ndings.ObstetGy- naecol1997; 89:184^192.
⢠BevanC.Pelvicin£ammatorydisease.RCOG,PersonalAssessmentin Continuing Education,1998.
Less commonly, infection of the upper genital tract may arise from direct spread from an area of intra abdominal sepsis, usually associated with the bowel, or rarely from blood-borne infection such as tuberculosis