Pelvic inflammatory disease 2

1
• This is a pure dedication to our beloved
professor “Dr.Usha Suresh” mam.
• Hope this ppt would benefit you with
certain new points.

PELVIC INFLAMMATORY
DISEASE
BLUE UNIT

DEFINITION
• Pelvic inflammatory disease is a
disease of sexually and
reproductively active women
used to describe the infection
and inflammation of the Upper
genital tract, with no mention of
the site or severity of infection

Contd..
• Involving any or all of the
uterus , oviducts and ovaries ;
this is often accompained by
involvement of the
neighbouring pelvic organs

• By definition,PID is a community
acquired infection intiated by the
sexually transmitted agent ,
distinguishing it from (RTI) pelvic
infections caused by transcervical
medical procedures, pregnancy
and other primary abdominal
processes that can extend to
pelvic organs

It is the most serious infection
in women aged 16-25 years and
the resultant morbidity exceeds
that produced by all other
infections combined for this age
group.

More specific terms like
endometritis, parametritis,
salpingitis, salpingoophoritis etc.
can be used when diagnosis is made
on laparotomy, laparoscopy,
endometrial biopsy etc.

Subacute(Silent) PID
• It is not a clinical diagnosis.
• Rather, it is an ultimate diagnosis given to
women with tubal factor infertility who
lack a history compatible with upper tract
infection.
• Subclinical episodes are particularly
common among oral contraceptive users.

Acute PID
• Acute clinical syndrome
caused by ascending spread of
microorganisms from vagina,
endocervix to endometrium,
fallopian tubes, ovary etc.

Chronic PID
• Resultant sequelae when PID
fails to resolve.
• Manifests in the form of
hydrosalpinx,chronic
pyosalpinx, chronic interstitial
salpingitis, tubo ovarian cyst,
tuberculous form etc.

DEFENCE MECHANISMS
Dr. NIDA FAROOQUI 1st year P.G.

A NEED FOR NATURAL DEFENCE 
MECHANISMS 
● The genital tract forms a continuous  
pathway from the exterior to the 
peritoneal cavity. 
● The close proximity of the
urethra 
and anus to the vaginal orifice.

VARIOUS DEFENCE MECHANISMS
●Vulva and perineum of mature  
women have an excellent inherent 
resistance to infection. 
 
●Secretion of Undecyclinic acid, a
fungicidal, by apocrine glands.

●An intact Hymen prevents
ascending 
infections; when a virgin girl presents 
with PID, it is usually tubercular in
nature. 
●Vaginal acidity plays a very important
role in inhibiting growth of bacteria;
attributed mainly to synthesis of lactic acid
by gram-positive anaerobic lactobacilli
from glycogen in cornified cells of vaginal
mucosa under the influence of oestrogen.

● Apposition of anterior and posterior 
walls of vagina.
 
● Unbroken epithelium due to
absence of 
glands.

● Phagocytic cells, cytokines, low
titres 
of antibodies. 
 
●Thick cervical alkaline mucus plug 
protective as a physical barrier and
also 
as a bacteriolytic.

●Uterine factors like the downward 
ciliary movement of the mucosal
lining 
in the uterus and cervical canal.
 
●Periodic shedding of the
endometrium 
during menstruation does away with
any infection which may try to gain
a hold.

●Non-pathogenic anaerobic streptococci
clear away the debris after menstruation
and pregnancy.

VARIATIONS IN THE EFFICIENCY 
OF DEFENCE MECHANISMS
WITH AGE 
• Extremes of ages where pH 
approaches 7. 
•Thin and atrophied epithelial  
linings.

WITH MENSTRUATION 
 
• Absent cervical mucous
plug. 
• Alkaline menstrual
discharge. 
 
Gonococcal infection if contracted 
during this time is likely to ascend
to 
the uterus and tubes.

DURING PUERPERIUM 
 
•Raw placental site.
 
•Breaks in epithelial linings
of 
the cervix and vagina.
 
•Bruised and devitalised
tissues.

•Discharge of liquor and lochia  
reduces vaginal acidity.
 
•degenerating blood clots and 
fragments of decidua offer a
nidus for infection.
 
•Lowered resistance due to
strain 
of pregnancy, anaemia etc.

MGMH
INCIDENCE & MICROBIOLOGY OF
PID
 
 
 
 
BY
- Dr. Vaishnavi Priyamsha
- Blue unit,MGMH
7/6/2015
24

MGMH
AGE and INCIDENCE
• Acute PID occurs in about 1-2% of young sexually active women.
• The incidence is 101000 sexually active women in the age
group of 15-39 years.
• The PEAK incidence occurs in age group of
15-24 years which corresponds to about 20/1000..
7/6/2015
25

PID Classification
Severe symptoms
4%
Mild to moderate symptoms
36%
Subclinical/silent
60%

MGMH
RISK OF PID WITH VARIOUS METHODS OF
CONTRACEPTION
• The risk of PID in a sexually active women without any
contraception is arbitrarily numbered as 1
• 2-4 with use of IUDS
• 0.4 with use of barrier contraceptives
• 0.3 with use of oral contraceptive pills
7/6/2015
27

MGMH
SPONTANEOUS Vs IATROGENIC
• 40-50% cases of PID develop spontaneously in young sexually active
women
• 50% cases of PID develop due to pelvic infections caused by medical
procedures,pregnancy,and other primary abdominal procedures.
7/6/2015
28

MGMH
INCIDENCE OF CHRONIC SEQUELAE OF PID
• RECURRENT PID:
• 12% -single episode of PID
• 35%-two episodes of PID
• 75%-three episodes of PID
7/6/2015
29

MGMH
• ECTOPIC PREGNANCY:The risk of ectopic pregnancy is increased
both with the increasing number and severity of PID.
• The ratio of ectopic to intrauterine pregnancy
• 1:15 after one episode of PID
• 1:6 after two episodes of PID
• 1:3 after three episodes of PID
• The ratio of ectopic to intrauterine pregnancy
• 1:35 with a single episode of MILD PID
• 1:25 with single episode of MODERATE PID
• 1:5 with single episode of SEVERE PID
7/6/2015
30

MGMH
• INFERTILITY:
• With increasing number of episodes of PID the pregnancy rates are
• 89 with one episode of PID
• 77 with two episodes of PID
• 48 with three or more episodes of PID
• The cumulative proportions of women achieving a LIVEBIRTH
• 90 after mild PID
• 82 after moderate PID
• 57 after severe PID
7/6/2015
31

MGMH
ORGANISMS RESPONSIBLE FOR PID
• SEXUALLY TRANSMITTED
• Neisseria gonococcus
• chlamydia trachomatis
• Mycoplasma
• Trichomonas
• AEROBES
• Staphylococcus
• Streptococcus
• E.coli
• Klebsiella
• ANAEROBES
• Bacteroides
• Fusobacteria
• Peptococci
• Peptostreptococci
• Clostridia
• Facultative anaerobes
• Actinomyces
• Mycobacterium
7/6/2015
32

MGMH
ORGANISMS RESPONSIBLE FOR PID
• Neisseria gonococcus and chlamydia trachomatis are the most
commonly identified pathogens in PID among sexually active
premenopausal females.
• E.coli and colonic anaerobes may be responsible for rare causes of
PID seen in post menopausal group..
• But the most cases of PID are result of poly microbial infection
caused by organisms ascending from vagina and cervix,to infect the
lining of endometrium and fallopian tubes,regardless of initiating
pathogens.
7/6/2015
33

MGMH
NEISSERIA GONOCOCCUS
• Morphology –organism is a gram negative diplococcus with adjacent
sides concave,being typically kidney shaped
• Gonococci posses pilli on their surface which facilitate their
adhesion to mucosal surface and promote virulance by inhibiting
phagocytosis
7/6/2015
34

MGMH
• The diagnosis can be proved by:- demonstration of gonococci on
smears
- culture
-NAAT
• The women should not have passed urine or used douche before
examination.
• Sites of specimen collection:
1]urethra :having its orifice wiped,urethra is milked to obtain
specimen fron para urethral glands.
2]bartholin glands and ducts.
3]endocervix.
4]anal canal and rectum.
7/6/2015
35

MGMH
• Gonococci will survive on ordinary swabs for aproximately 2hours.
• A longer interval between sample collection and their arrival at
laboratory requries transport medium:STUART’S AGAR
• The selective media for neisseria gonorrhea:THAYER-MARTIN
MEDIUM
7/6/2015
36

MGMH
CHLAMYDIA TRACHOMATIS
• MORPHOLOGY:chlamydia is an obligate intracellular bacterial
parasite.
• Gram negative
• Chlamydia occur in two forms :-elementary form
-reticulate form
7/6/2015
37

MGMH
• SPECIFIC TESTS: -culture
• -DFA [direct floroscent antibody]
-NAAT [nucleic acid amplification tests]
• -ELISA [enzyme linked immunosorbent assay]
7/6/2015
38

MGMH
• SAMPLE should be taken with cotton-tipped swabs,which after
mopping should pick up columnar epithelial cells from exduate
• Culture media:6-8 days old chick eggs
cell lines,sucha as McCOY/HeLa cell lines
• ELISA preffered method for screening
• NAAT,such as PCR,have a greately increased sensitivity,specifity
advantage:non invasive samples such as urine samples
can be used.
7/6/2015
39

MGMH
• The type and number of species vary depending on stage of disease
• Gonococci are often cultured from cervix during 24-48 hours of
disease,which are absent later
• Late in disease anerobic organisms predominate
• -bacteroides
• -peptococcus
• -peptostreptococcus
7/6/2015
40

MGMH
PUERPERAL and POST ABORTAL PID
Causative organisms
-streptococcus
-staphylococcus
-E.coli
-mycoplasma
-chlamydia
7/6/2015
41

PATHOGENESIS OF PELVIC
INFLAMMATORY DISEASE
-DR.NILOFER SHAHEEN

RISK FACTORS OF PID
➢ MENSTRUATING TEANAGERS
➢ MULTIPLE SEXUAL PARTNERS
➢ AGE AT FIRST INTERCOURSE
➢ FREQUENCY OF INTERCOURSE
➢ PREVIOUS HISTORY OF ACUTE PID
➢ IUCD USERS
➢ AREAS WITH HIGH PREVALENCE OF PID

RISK FACTORS…
➢HSG
➢DILATATION AND CURRETAGE
➢MANUAL REMOVAL OF PLACENTA
➢SOCIOECONOMIC STATUS
➢SMOKING

PROTECTIVE FACTORS
➢OC PILLS
➢TUBAL LIGATION
➢BARRIER CONTRACEPTIVES
➢PREGNANCY

MODES OF SPREAD OF INFECTION
➢THROUGH CONTINUITY AND CONTIGUITY
➢THROUGH LYMPHATIC AND PELVIC VEINS
➢THROUGH BLOOD STREAM
➢FROM ADJACENT INFECTED EXTRAGENITAL
ORGANS

➢THROUGH CONTINUITY AND
CONTIGUITY
➢FROM ADJACENT INFECTED EXTRAGENITAL
ORGANS

48
PATHOPHYSIOLOGY of Ascendant
Infection
Cervicitis
Endometritis
Salpingitis/
oophoritis/ tubo-
ovarian abscess
Peritonitis
Pathogenesis

• NONTUBERCULOUS PID
• GONOCOCCAL NON
• GONOCOCCAL
•
• CHLAMYDIA
• MYCOPLASMA
• AEROBIC
ORGANISMS
• ANAEROBIC
ORGANISMS

• N.GONOCOCCUS :
• RAPID GROWTH CYCLE OF 20-40 MINS
LOGARITHMIC INCREASE OF ORGANISMS
RAPID AND INTENSE INFLAMATORY RESPONSE
MIGRATION OF BACTERIAL PRODUCTS TO
PERITONIAL CAVITY AND VAGINA CAUSES
SYMPTOMS OF PID

• CHLAMYDIA: SLOW GROWING
INTRACELLULAR ORGANISM.
• GROWTH CYCLE IS 48-72 hrs
• SLOW GROWTH DOES NOT INDUCE RAPID
INFLAMATORY RESPONSE.
• DUE TO INTRACELLULAR GROWTH, RELEASE
OF ELEMENTARY BODIES OCCUR BY RUPTURE
OF CELL THAT IT HAS INVADED.
• REPEATED OCCURRENCE OF ELEMENTARY
BODY INFECION OF SUSCEPTIBLE CELLS AND

THEIR SUBSEQUENT DESTRUCTION BY
RUPTURE IS THE MAJOR MECHANISM BY
WHICH CHLAMYDIA CAUSES DISEASE
TISSUE DAMAGE PROVIDES FERTILE GROUND
FOR GROWTH OF SECONDARY INFECTING
ORGANISMS
IT CAUSES INFLAMMATION AND FIBROSIS OF
SUBMUCOSA AND MUSCULARIS AND THUS
MORE PERMANENT DAMAGE.
IT CAUSES INCREASED INCIDENCE OF CHRONIC
PELVIC PAIN,ECTOPIC AND INFERTILITY

56
Normal Human Fallopian Tube Tissue
Source: Patton, D.L. University of Washington, Seattle, Washington
Pathogenesis

57
C. trachomatis Infection (PID)
Source: Patton, D.L. University of Washington, Seattle, Washington
Pathogenesis

ACUTE SALPINGITIS
• FALLOPIAN TUBE IS SWOLLEN,
OEDEMATOUS,HYPEREAMIC WITH VISIBLE
DILATED VESSELS
• MUCOSA IS OEDEMATOUS, INFILTRATED
WITH LEUCOCYTES AND PLASMA CELLS.
• INFLAMMATORY EXUDATE IS DISCHARGED
INTO LUMEN MAINLY AMPULLA
• ULCERATIONS OF MUCUSA CAUSES
ADHESIONS AND TUBAL BLOCKAGE

• WHEN FIMBRIAL END IS NOT CLOSED PUS
POURS INTO PELVIC CAVITY-SURE SIGN
OF PID
• WITH SEALING OF FIMBRIAL END BY
FIBRINOUS ADHESIONS, PUS
ACCUMULATES IN TUBAL
LUMEN,FORMING TUBAL ABSCESS
• WITH INVOLVEMENT OF OVARY,
TUBOOVARIAN ABSCESS OR MASS IS
FORMED,ENTANGLED IN ADHESIONS.

• ACUTE PHASE OF INFECTION IS FOLLOWED
BY
• RESOLUTION-IF INFECTION DOES NOT
CAUSE APPRECIABLE TISSUE DESTRUCTION
• ABSCESS FORMATION- ENDOSALPINX IS
DESTROYED AND CONVERTED INTO
GRANULATION TISSUE,PUS IS FORMED
LEADING TO TUBAL ABSCESS
• HEALING BY FIBROSIS-TUBAL WALL
THICKENS,PLICAE ADHERE TO DISTORT
LUMEN

• TUBES AND OVARY ADHERE TO ADJACENT
ORGANS
• HYDROSALPINX- WHEN INFLAMMATION
SUBSIDES WITH FIMBRIAL END SEALED AND
TUBAL EPITHELIUM IS INTACT, SECRETIONS
ACCUMULATE.
• CORNUAL END IS OPEN.
• MUSLE IS DAMAGED AND STETCHED,TUBE
DRAINS INTO PERITONIAL CAVITY
• FLATTENING OF TUBAL PLICAE OCCURS
WITH EXFOLIATION OF EPITHELIUM
• TUBOOVARIAN ABSCESS

THROUGH LYMPHATICS AND PELVIC
VEINS
• SPREAD OF PUERPERAL AND POST ABORTAL
INFECTIONS
CERVICITIS
VIA LYMPHATICS
EXOSALPINGITIS
PERITUBAL AND PERIOVARIAN ADHESIONS
AND THICKENED TUBAL WALL

THROUGH BLOOD STREAM
• GENITAL TUBERCULOSIS OCCURS ALMOST
ALWAYS SECONDARY TO A PRIMARY FOCUS
ELSEWHERE.
• MODE OF SPREAD IS GENERALLY
HEAMATOGENOUS.
• ONCE GENITAL TRACT IS
COLONISED,GRANULOMATA CONTAINING VIABLE
TUBERCLE BACILLI IS FORMED.
• FOLLOWING THE DEVELOPMENT OF
TUBERCULAR HYPERSENSITIVITY,THESE FOCI
BECOME SILENT

• THE ACTIVE GROWTH AND INCREASE IN
BLOOD SUPPLY TO GENITAL ORGANS AROUND
MENARCHE LEADS TO REACTIVATION OF THE
DISEASE
• WHEN THE TUBERCLE BACILLY INFECT A
HOST ,INITIAL REACTION IS
POLYMORPHONUCLEAR EXUDATE
• WITHIN 48hrs,THIS IS REPLACED BY
MONONUCLEAR CELLS,SITES FOR
INTRACELLULAR TUBERCLE REPLICATION
• AS CELLULAR IMMUNITY
DEVELOPS,DESTRUCTION OF TUBERCLE
BACCILY BEGINS, LEADING TO CASEATION
NECROSIS

• LATER REACTIVATION OF THE LESION
LEADS TO CLASSICAL GRANULOMATOUS
LESION(CENTRAL CASEATION AND
NECROSIS SURROUNDED BY EPITHELIOID
CELLS,GIANT CELLS,MONOCYTES AND
LYMPHOCYTES)

• TB OF FALOPIAN TUBE:
*HEMATOGENOUS SPREAD.
• TUBAL MUCOSA IS FAVOURABLE NIDUS
RESULTING IN
ENDOSALPINGITIS(BILATERAL)
• TUBES ARE ENLARGED IN DIAMETER
WITH THEIR EXTERNAL SURFACE
ROUGHENED DUE TO ADHESIONS AND
SHOW GREYISH TUBERCLES
• ON CUT SECTION LUMEN SHOWS THE
PRESENCE OF CASEOUS MATTER

• LEAKAGE OF INFECTED MATERIAL LEADS
TO PERITUBAL ABSCESS,TB PERITONITIS
AND ASCITES
• AS DISEASE ADVANCES ,REACTIVE
FIBROSIS SETS IN AND TUBES GET
OCCLUDED
• FOLLOWING DIRECT
SPREAD,EXOSAPINGITIS MANIFESTS AS
DIFFUSE MILIARY TUBERCLES,AMPULLA IS
DILATED WITH FIMBRIAL END OPEN AND
POUTING(TOBACCO POUCH APPEARANCE)

• TB OF ENDOMETRIUM(50%):
TRANSLUMINAL SPREAD(DESCENDING
INFECTION)
• HISTOLOGY REVEALS CASEATING
GRANULOMAS
• CAVITY APPEARS SHRUNKEN
• TUBAL OSTIA APPEARS LIKE GOLF HOLES
• TOTAL DESTRUCTION OF ENDOMETRIUM MAY
OCCUR RESULTING IN AMENORRHOEA
• PYOMETRA FORMATION MAY OCCUR
• THE CAVITY MAY BE OBLITERATED WITH
INTRAUTERINE ADHESIONS(ASHERMANS
SYNDROME)

• TB OF OVARIES(20-30%): SPREADS
FROM FALLOPIAN TUBE.
• PERIOOPHORITIS OCCURS RESULTING IN
ADHESIONS.
• FOLLOWING HAEMATOGENOUS
SPREAD,CASEATING GRANULOMAS ARE
FORMED WITHIN THE PARENCHYMA OF
OVARY

➢THROUGH CONTINUITY AND CONTIGUITY
➢FROM ADJACENT INFECTED
EXTRAGENITAL ORGANS

FROM ADJACENT INFECTED
EXTRAGENITAL ORGANS
• APPENDICITIS OR DIVERTICULITIS
• PELVIC PERITONITIS
• SALPINGITIS
• IT’S A MIXED INFECTION,MAINLY CAUSED
BY COLIFORM ORGANISMS AND GRAM
NEGATIVE ENTEROBACTERIACAE

STAGES OF PID
• STAGE 1- ACUTE SALPINGITIS WITHOUT
PERITONITIS(NO ADHESIONS)
• STAGE 2- ACUTE SALPINGITIS WITH
PERITONITIS(PURULENT DISCHARGE)
• STAGE 3-ACUTE SALPINGITIS WITH
SUPERIMPOSED TUBAL OCCLUSION OR
TUBOOVARIAN COMPLEX
• STAGE 4- RUPTURED TUBOOVARIAN
ABSCESS
• STAGE 5- TUBERCULAR SALPINGITIS

Pelvic Inflammatory Disease 
(signs &symptoms,diagnosis, 
differential diagnosis)
- Reshma M

Subclinical (Silent) PID
• Study:
– In 112 infertile women,
• 36 had adhesions or distal tube occlusion suggestive of PID by laparoscopy
• 11 had a history of this diagnosis.
• In addition, up to one-third of women without a history of PID harbour persistent
C.trachomatis in the upper genital tract despite the absence of clinical findings
except infertility
• Based on these observations, it seems clear that subclinical PID
is severe enough to produce significant sequelae

• Histologically - presence of neutrophils and plasmacells in
endometrial tissue
• Many of these patients have antibodies to C.trachomatis and/or
N.gonorrhoeae.
• Laparoscopy or laparotomy - may have evidence of prior tubal
infection such as adhesions,but for the most part,the fallopian tubes
are grossly normal.
• Internally - however, there are flattened mucosal folds ,extensive
deciliation of epithelium,and secretory cell epithelial degeneration.
• Alternatively hydrosapinx may be found.
• Fine adhesions between the liver capsule and anterior abdominal
wall may also be evidence of prior silent disease

Presentation of acute PID
❑ Onset is usually during or shortly after menses
❑ H/O previous abdominal and /or gynaecological surgeries
❑ H/O IUCD usage
❑ Sexual and STDs history and partner’s STDs history
❑ Symptoms-
• Lower abdominal pain - cardinal presenting symptom
– In more than 90% of patients, at initial presentation
– It is of recent onset ,usually less than 7days
– Usually described as bilateral, constant and dull and is
accentuated by motion and sexual activity

• Fever
• Nausea and vomiting in case of peritonitis
• Abnormal vaginal discharge,postcoital bleeding and
symptoms suggestive of dysuria in case of sexually
transmitted infections
• Menstrual irregularities if it is due to preceding
endometritis
• Severe diarrhoea due to rectal irritation in case of
pelvic abscess

❑ On physical examination,
➢ High temperature (Oral temperature >101⁰F or 38.3⁰C)
➢ Tachycardia
➢ Tongue showing signs of dehydration
❑ On abdominal examination,
➢ Diffuse tenderness greatest in lower quadrants,which may or
may not be symmetrical
➢ Rebound tendreness ,rigidity and decreased bowel sounds
➢ In some cases- marked tenderness in the right upper abdomen-
may suggest Fitz-Hugh Curtis syndrome

• Perihepatitis (fitz-Hugh curtis syndrome):
✓ Can be a complication of gonococcal or chlamydial salpingitis
✓ Occurs in 1-10% cases of acute PID
✓ Classically manifests with sharp pleuritic upper quadrant pain
that accompanies pelvic pain
✓ It manifests as a patchy purulent and fibrinous exudate in the
acute phase(violin string adhesions),most prominently affecting
the anterior surfece of the liver(not the liver parenchyma)
✓ May be confused with acute cholecystitis or pneumonia

• If all abdominal quadrants are involved , ruptured tubo ovarian
abscess should be suspected
• It is rare for an abdominal swelling to be palpated in acute
cases
❑ On pelvic examination,
per speculum
– Mucopurulent endocervical discharge
– A torn cervix or damaged tissue is evident in post abortal sepsis and
criminal abortion

Bimanual pelvic examination
– Cervical motion and adnexal tenderness
– Other diagnoses should be considered if uterine and
adnexal tenderness are not prominent
– Pelvic abscess produces a fluctuating tender swelling
in the pouch of Douglas, bulging into the posterior
fornix

• PID is difficult to diagnose accurately, in part, because
manifestations range from mild to quite severe
• All young sexually active women presenting with lower
abdominal pain should be carefully evaluated for the
presence of salpingitis and endometritis

Investigations
❑ Laboratory tests
• Pregnancy test
• to rule out ectopic pregnancy and complications of
intrauterine pregnancy
• Complete blood picture with erythrocyte
sedimentation rate
➢Although PID is usually an acute process, less than half of
PID patients exhibit leucocytosis

➢ ESR - non-specific and is a crude indicator of severity of disease
-elevated >15mm/hr in about 75% of women with
laparoscopically confirmed acute salpingitis
- also elevated in 53% of women with pelvic pain and normal
appearing pelvic organs
• Microscopic examination of vaginal discharge in saline
One study of 120 women showed that increased white blood
cells in vaginal fluid was the most sensitive laboratory test for
PID. However, specificity was only 39%.

• Gram-stained endocervical smear(to quantify PMNs/
1000x field and to look intracellular gram-negative
diplococci)
If a cervical gram stain is positive for gram negative
intracellular diplococci when interpreted by an
experienced microscopist, the probability of PID
greatly increases; if negative it is of less use

• Endocervical NAAT (Nucleic Acid Amplification Test)/
endocervical(or rectal) cultures for N.gonorrheae
• Culture of endocervical swab/NAAT for endocervical swab or
first void urine for C.trachomatis
• Urinanalysis
• C-reactive protein(optional)
• HIV testing
• Hepatitis B surface antigen and surface antibody
• Testing for syphilis
• Decreased or absent isoamylase in peritoneal fluid is the best
non-culture laboratory test for the disease

3.Positive “whiff test”(Amine Test)
Release of fishy amine odour on
addition of 10% KOH to the discharge
Also observed in trichomonas infection
4.Clue cells on saline wet mount of vaginal
discharge(on >20% cells)
Bacteria adhered to epithelial cells;
most reliable single indicator
Clinical diagnostic criteria for bacterial vaginosis 
(Amsel’s criteria)
Must have atleast 3 of the following findings-
1.Characteristic vaginal discharge-
Creamy greyish white, homogenous discharge adherent to vaginal walls
2.Vaginal pH >4.5
High sensitivity;Poor specificity (false positive with mucus, menses,
semen)

Laboratory examination of vaginal smears and
determination of Nugent Score
N score =sum of the score for each bacterial morphotype listed
below(Note number of organisms seen/100x objective)
Large gram
positive
rods(lacto
bacilli
spp.)
SCORE Small gram
variable
rods(G.vag
inalis,bact
eroids
spp.)
SCORE Curved
gram
variale
rods(mobil
incus spp.)
SCORE Sum=N
SCORE
30 or > 0 0 0 0 0 0
5-30 1 <1 1 <1 1 3
1-4 2 1-4 2 1-4 1 5
<1 3 5-30 3 5-30 2 8
0 4 30 or > 4 30 or > 2 10

Interpretation of Nugent Score
If N Score is: AND Then report:
0-3 Smear NOT consistent
with BV
4-6 Clue cells not present
4-6 Clue cells are present Smear consistent with
BV
7-10

Imaging Techniques
▪ Ultrasonography - normal fallopian tubes are rarely
imaged;characteristic findings include
✓ Distended,ovoid shaped tube filled with anechoic or echogenic fluid
✓ Fallopian tube wall thickening
✓ Incomplete septa
✓ A “cogwheel” appearance when inflammed tubes are imaged in
cross section
Sonography may also be used to identify tuboovarian abscess or to
exclude other pathology as the pain source

Endometritis (thickened heterogenous endometrium)

Pelvic inflammatory disease and tuboovarian complex. 
A) Sagittal endovaginal sonogram reveals complex free fluid (FF). U = uterus. 
B) Coronal image of left adnexa reveals dilated fallopian tube (T) with echogenic fluid.
Findings are consistent with those of pyosalpinx.

▪ Doppler-colour and power doppler will show increased flow in
the walls and septa with both pyosalpinx and tuboovarian
abscess
Endovaginal sonogram reveals tubular structure with debris in left adnexa
; finding is compatible with pyosalpinx

▪ Computarised tomography and Magnetic resonance
imaging-
useful with both pyosalpinx and tubovarian mass if
sonography
does not lead to clear diagnosis

▪ Chest x-ray and upper abdominal sonography - in women
with right
upper abdomen quadrant pain to exclude other pathology
Note thin rim of fluid underneath the diaphragm above the liver in a patient
with PID presenting with acute right upper quadrant pain radiating to the right
shoulder, Fitz-Hugh-Curtis Syndrome

❑ Endometrial biopsy –
Polymorphonuclear leucocytes on the endometrial surface
correlate with acute endometritis,whereas plasma cells
correlate with chronic endometritis
– It does not provide useful information to alter the diagnosis and therapy
Micrograph showing a chronic endometritis with the characteristic plasma cells.
Scattered neutrophils are also present. H&E stain

Plasma cell endometritis (PCE)
✓ PCE occurs among asymptomatic women with no others
evidence of PID
✓ It has been identified as an important component of PID
✓ The density of plasma cell infiltrate correlate with the
clinical severity of disease
✓ The specificity of endometritis for the diagnosis of PID
was 92% with a positive predictive value of 77%

❑ Laparoscopy
– Subsequent studies from the 1990s found the sensitivity of
laparoscopy to be as low as 50% with specificity
approaching 100%
– Thus laparoscopy has substantial value in confirming the
diagnosis but is not sensitive enough to be a diagnostic gold
standard
Laparoscopy for the following
✓ A sick patient with suspicion of a competing
diagnosis(usually appendicitis etc.)
✓ An acutely ill patient who has failed outpatient treatment
for PID
✓ Any patient not clearly improving after approximately 72
hours of inpatient treatment for PID

Laparoscopy image and close-up image of same patient showing
sausage-shaped dilated right fallopian tube

CDC Criteria For The Diagnosis of
Acute Salpingitis
• Empirical treatmant of PID should be intiated in sexually
active young women and other women at risk for STDs if
they are experiencing pelvic or lower abdominal
pain,if no cause for the illness other than PID can be
identified,and if one or more of the following minimal
criteria are present on pelvic examination:
➢ Cervical motion tenderness
➢ Uterine tenderness
➢ Adnexal tenderness

Additional criteria to enhance the specificity of
minimum criteria and to support a diagnosis of PID
➢ Oral temperature >101⁰F(>38.3⁰C)
➢ Abnormal cervical or vaginal mucopurulent discharge
➢ Presence of abundant numbers of WBC on saline microscopy of
vaginal secretions
➢ Elevated ESR
➢ Elevated C-reactive protein
➢ Laboratory documentation of cervical infection with
N.gonorrhoeae or C. trachomatis

The most specific criteria for diagnosing PID include the
following:
➢Endometrial biopsy with histopathological evidence of
endometritis
➢Transvaginal sonography or magnetic resonance imaging
techniques showing thickened,fluid-filled tubes with or
wihtout free pelvic fluid or tuboovarian complex,or Doppler
studies suggesting pelvic infection(eg.,tubal hyperemia)
➢Laparoscopic abnormalities consistent with PID

Differential diagnosis of Acute Pelvic
Inflammatory Disease
❑ Gynaecological
– Dysmenorrhea
– Incomplete or complete abortion
– Ovarian torsion
– Ectopic pregnancy
– Tuboovarian abscess
– Mittelschmerz
– Ovarian mass
– Prolapsing leiomyoma
– Outflow tract obstruction

❑ Gastrointestinal
– Gastroenteritis
– Colitis
– Irritable bowel disease
– Appendicitis
– Diverticulitis
– Inflammatory bowel disease
– Constipation
– Small bowel obstruction
– Mesenteric ischemia
– Gastrointestinal malignancy

❑ Urological
– Cystitis
– Pyelonephritis
– Urinary tract stone
– Perinephric abscess
❑ Musculoskeletal
– Hernia
– Peritonitis
– Abdominal wall trauma

❑ Miscellaneous
– Diabetic ketoacidosis
– Herpes zoster
– Opiate withdrawal
– Hypercalcemia
– Sickle cell crisis
– Vasculitis
– Abdominal aortic aneurysm rupture
– Abdominal aortic aneurysm dissection
– Porphyria
– Heavy metal toxicity

MEDICAL MANAGEMENT OF
ACUTE PID

➢Reproductive tract infections & STI’s are an important
public health problem in India
➢6% adult Indian population are suffering from RTI’s
Medical management of acute PID

Syndromic case management 
SCM is a comprehensive approach for STI/RTI’s control
Endorsed by WHO
● Syndromic case management approach classifies STI’s /RTI’’s
into syndromes (these are easily identifiable groups of symptoms
& signs) and provides treatment for most common organisms
causing syndrome
● Diagnosis based on the identification of syndrome
● Which are combination of the symptoms the client reports
and signs the clinician observes
● It provides treatment on the first visit
● low threshold for empiric treatment of PID is
recommended because of the lack of definitive clinical
diagnostic criteria &because the potential consequenses of
not treating of PID are significant

● The syndromic case management achieves high cure
rates because it provides immediate treatment on the first
visit at little /no laboratory cost
● Provides single dose treatment as far as possible
● The recommended treatment is effective for all the diseases
● It includes 4C’’s
● Condom demonstration and promotion
● Ensuring compliance with treatment
● Counseling
● Contact treatment/partner management

WHY SYNDROMIC APPROACH
● STI/RTI signs and symptoms are rarely specific to a
particular disease
● Laboratories are non functional due to lack of resources
● Dual infections are quite common
● Failure of cure at first contact

GOALS OF MANAGEMENT OF PID
● Elimination of acute infection & symptoms
● Prevention of long term sequale such as infertility ectopic
pregnancy chronic pelvic pain

Clinical cure
● Significant improvement in the signs and symptoms
Microbial cure
● Eradication of N.gonorrhoea/C.trachomatis
● If present at base line

TREATMENT
● Outpatient therapy –mild to moderate PID
● Inpatient therapy-severe PID
OUT PATIENT THERAPY
● The CDC recommends any of the following with/without
metronidazole( 500mg twice a day for 14 days
Ceftriaxone 250 mg IM single
dose
+
Doxycycline 100 mg orally
twice a day for 14 days

a single
dose
+
doxycyclin
e 100mg
orally
twice a day
for 14 days
Cefoxitin 2g IM in a single dose
With
Probenacid 1g orally in a single dose
+
Doxycycline 100 mg orally twice a day for
14 days
Other regimens
Cefotaxime(1g IM in a single dose)
Or
Ceftizoxime (1g IM in a single dose)
+
Doxycycline(100mg orally twice a day for
14 days

● Metronidazole causes gastrointestinal side effects will
lead to non adherence &inadequately treted PID
Inclusion of anaerobic coverage
● Severe infection requiring hospitalization
● Tuboovarian abscess
● h/o gynecological instrumentation within the preceding
2-3 weeks

● Ceftriaxone has best activity against gonococcal infection
● Fluoroquinolones are no longer recommended for the
treatment of Gonorrrhoea
● Azithromycin [1g once /week]and doxycyccline were found to
equalent in clinical cure rates
● Reevaluation of the patient within 48 hrs to 72hrsof
initiating therapy to determine response of disease such as
reduction in abdominal tenderness & cervical tenderness

● If no clinical improvement has occurred within 72 hrs requires
● Hospitalization
● Parenteral therapy
● Further diagnostic evaluation

Indications for hospitalization
● Surgical emergencies such as appendicitis
● Pregnancy
● Lack of response or tolerance to oral medication
● Inability to take oral medication due to
nausea & vomiting
● Severe clinical illness
● Complicated PID with pelvic abscess

● Inpatient therapy
First line regimen
CDC recommends either of the following
Cefoxitin 2gIV 6th hrly
Or
Cefotetan 2g IV 12th hrly
with
Doxycycline 100 mg orally twice
daily

● Clindamycin 900mg IV every 8th hrly
Plus
Gentamycin loading dose2 mg/kg body weight followed by
maintenance dose started 1.5mg kg body wt every 8th hrly
● These inpatient regimen provides broad coverage including
streptococci Gram negative enteric bacilli [ E.coli Klebsiella &
Proteus]anaerobic organisms
● Transitioning from parenteral to oral therapy can usually
started after 24hrs of sustained clinical improvement
● Patient should complete a 14 day course of treatment with
doxycycline

AITERNATIVE REGIMENS
● Ampicillin – sulbactum + doxycycline
● Azithromycin monotherapy
● Azithromycin metronidazole
● h/o mild allergy to penicillin ceftriaxone can be used
● h/o severe allergy
● Clindamycin + Gentamycin
● Levofloxacin{500mg OD 14days}
● Azithromycin
● moxifloxacin

● Intravenous fluid therapy
● Analgesia
● Antiemetic and antipyretic treatment
● FOWLERS POSITION
● This position facilitates collection of pus in the pouch
of douglas

Patient Monitoring
● A Chart has to be maintained for monitoring
● It contains daily recordings of
● Temperature
● Pulse rate
● Blood pressure
● abdominal examination
● Pelvic examination for cervical movement tenderness
● Every 3day ESR & CRP
● If no clinical improvement within 72 hrs diagnostic evaluation
is recommended

Efficacy of inpatient versus outpatient
therapy
● PEACH[The Pelvic inflammation Disease Evaluation
Clinical Health trial]
● The clinical trial showed that short term clinical and
microbiological outcomes and longterm reproductive
outcomes are similar between intravenous and oral
therapy
● In this trial intravenous therapy continued for 48hrs
upon clinical improvement the ptn was switched to
doxycycline for 14 days

Partner treatment
Male sexual partner of PID should be examined
and treated if they had sexual contact with the patient
during previous 60 days prior to the onset of symptoms
regardless of test results
•Male partners of women who have PID caused by
C.trachomatis &N.gonorrhoea frequently asymptomatic
•Ceftriaxone 250 mg IM
+
Azithromycin[1g]orally /doxycyclineorally twice daily
for 7 days

PID Special situation
Pregnant patients
● Infection can occur in first 12weeks of pregnancy
cefoxitin /cefotetan IV
+
Azythromycin{instead of
doycycline}

IUD Users
● Risk of PID assocciated with IUD use is primarily confined to
first 3 weeks after insertion and is uncommon there after
● If improvement is not seen within 72hrs of starting treatment
then removal of IUCD considered
Post menopausal women
Rare in these patients
Extragenital pathology in addition to genital tract malignancies
Most commonly due to iatrogenic causes
Most commonly E.coli & klebsiella found
Tubo ovarian abscess is common

Treatment
● Inpatient and parenteral treatment
● Surgical exploration if patient is not improving in 48 hrs
WOMEN WITH HIV
● Women with PID who also infected with HIV should be
treated with the same antibiotic regimen as women who are
HIV negative

Counseling &screening
● Clinician should counsel regarding partner treatment and
future safe sexual practices
● All patients with acute PID should be offered HIV testing
● Assessment of immunity to hepatitis virus vaccination of
those who have no evidence of immunity

● Serological testing for syphilis
● Patients who are through 9 to 26 yrs of age should offered
immunization against HPV infection
● Drug abuse counselling

KIT 6
● Cefixime 400mg single dose
● Metronidazole 400mg for 14 days
● Doycycline 100mg for 14 days

Follow up
Further review 4 to 6 weeks after therapy may be useful
to ensure
● Adequate clinical response to treatment
● Compliance with oral antibiotics
● Screening and treatment of sexual contacts
● Awareness of significance of PID and its sequale
● That a repeat pregnancy test is negative if clinically
indicated
● If a women is likely to be risk of future PID and
requests an IUD for contraception , the LNG-IUS
would be the most appropriate choice

SEVERE PID AND SEQUELAE
CHRONIC PID
Dr.Sirisha

SEVERE PID
! Stage III
Acute salpingitis with superimposed “tubal
occlusion” or “tuboovarian complex.”
! Stage IV
Ruptured tubo-ovarian abscess.

Clinical diagnosis of acute
PID
TAS and
TVS**
Evidence of adnexal mass
(thick walled irregular cystic lesion, thick
internal septations, debris
and internal echoes)
STAGE-III

Management:
Investigations
Pregnancy test
☞Hb%
☞WBC count : leucocytosis
(inc.neutrophils)
☞Basic surgical profile
☞special Ix : TVS

STAGE-III
ANTIMICROBIAL THERAPY
CLINICAL CONDITION
IMPROVEMEN
T
STAGE
IV

Stage IV - RUPTURED TOmass
sudden, severe progression of pelvic pain
O/E :
seriously ill , dehydrated
Temp >101F (can be normal or subnormal in
late phase)
tachycardia
shallow and rapid respirations
hypotension (if 3rd space loss+)
P/A :
diffuse tenderness,rigidity,guarding
bowel sounds may be absent

X-RAY :
paralytic ileus with e/o free fluid in abdominal cavity.
CT :
pelvic abscess with free purulent fluid in upper abdomen.

Failure to respond in 48 -72 hrs  
Size >10cm
“PELVIC ABSCESS
DRAINAGE”
STAGE III disease

PELVIC ABSCESS DRAINAGE
MODALITIES:
1. Posterior colpotomy
2. Percutaneous abscess drainage
3. Laparoscopic drainage
4. Laparotomy and drainage

POSTERIOR COLPOTOMY
REQUIREMENTS :
Abscess should be in the midline or
nearly so.
It should be adherent to the cul-de-
sac peritonium and should dissect the
rectovaginal septum.
It must be cystic or fluctuant.

PROCEDURE
Patient is placed in lithotomy position
Under anaesthsia;pelvic examination is done to exactly know the size and
location of abscess

Posterior lip of cervix held with tenaculum and drawn downward and
forward.
An icision made on vaginal mucosa of posterior fornix and widened with a
pair of ling scissors
Minimum icision : 2cms for adequate drainage

Cul de sac peritoneum and abscess cavity are punctured with a long kelly
clamp(sign of entry-definite sensation of giving way into cystic caviy)
When abscess wall is punctured,blood or pus is usually seen in upper vagina.
Jaws of the clamp are spread to allow free flow from abscess cavity

It is desirable to explore the cavity by inserting index finger and release any
fibrous adhesions;to ensure complete drainage.
One or two drains can be placed into abscess cavity and allowed to drain for
4-6 days
CAUTION : avoid intraperitoneal spillage and bowel injury.

PERCUTANEOUS ABSCESS DRAINAGE
❑USG or CT guided.
❑Minimally invasive
❑USG
transvaginal/transabdominal

LAPAROSCOPIC DRAINAGE
Diagnostic role
In stage III - confirm the diagnosis when in doubt
- rule out other surgical emergencies
- identify other non infectious causes
which doesn’t respond to antibiotics.
Therapeutic role
-adhesiolysis
“ABSCESS DRAINAGE”
Disadvantage : Abscess cant be drained completely and risk of intraperitoneal spillage is
high.

LAPAROTOMY AND ABSCESS DRAINAGE
less preferred over laparoscopy.
*AIM : drain the pus and remove the source.
Position : lithotomy
Incision : lower transverse maylard incision
(adequate exposure of adnexa and pelvic side walls.)
Adhesiolysis
Bowel packin
Pelvic dissection Pus drainage

If bilateral adnexa involved TAH + BSO
In U/L involvement with opposite tube and ovary
NORMAL
U/L SALPINGO-OOPHORECTOMY (especially in
young women desirous of fertility)
---risk of recurrence in opposite adnexa***

Stage IV
Spontaneous rupture of pelvic abscess
RECTUM BLADDER PERITONEAL
CAVITY
Rectum :
improvement in clinical condition
drainage of pus through anus.
posterior colpotomy “NO”

Bladder :
secondary urinary infection
Laparotomy,abscess drainage and repair of
bladder wall.
Peritoneal cavity
Septic peritonitis(generalised)
(when delayed)
SEPTIC SHOCK (life threatening)

Stage IV
IMMEDIATE LAPAROTOMY is the need of
the hour.
shorter the interval b/n rupture and surgery, better
the outcome.
Pre-op phase:
1. Broad spectrum IV antibiotics
2. Cross matched blood 2-4 units
3. IV crystalloids
4. Urethral catheterisation (I/O charting)
5. CVP monitoring
6. ABG analysis and o2 inhalation if needed.

Operative phase :
To be performed as “rapidly” as possible.
Position :
Supine (avoid trendelenburg till abdomen is
packed.)
Incision :
lower midline incision; can be extended above
umbilicus if needed. (Allows rapid access)

Abdomen opened
“ODOUR”
(putrid and unpleasant)
PUS COLLECTED
(sent for gram staining, aerobic and anaerobic
C/S)
REMOVE THE SEPTIC FOCUS
(TAH + BSO)

EXPLORE THE UPPER ABDOMEN
(Look for pus in subdiaphragmatic and subhepatic spaces)
ABSCESS + NO
ABSCESS
Closed suction drainage
through upper abdominl wall
ABDOMINAL CAVITY IRRIGATION with warm
sterile saline

INCISION IRRIGATED WITH WARM SALINE
! Closed usually with continuous suture
! Retention sutures applied if necessary
! in case of gross contamination;skin and fat
left open and daily dressing done.
! in 4-5 days if tissues healthy closed by
secondary suturing.
TECHNICAL DIFFICULTIES :
Distorted anatomic landmarks
Dense adhesions
Thick edematous and friable tissues
Difficulty in hemostasis

INJURIES :
Bowel
serosal damage
perforation
*careful dissection of adhesions is required.
soft and fresh adhesions: blunt finger dissection
dense and fibrotic adhesions : sharp dissection
Ureteric injury
careful retroperitoneal dissection and ureter
identification.
*preoperative ureteric stenting may be required in
extensive damage.
*intraoperatively-indigo caramine test

If the patient is YOUNG and desiring FERTILITY
when rupture is strictly from U/L tuboovarian
abscess
opposite adnexa is realtively normal
U/L Salpingo - oophorectomy
IVF
*In majority of the cases; opposite adnexa is significantly
involved,hence recurrence is high,fertility is low,repeat
surgeries are high.
Post operative phase :
Should be monitored for sepsis,haemodynamic and
metabolic stability.

COMPLICATIONS AND LONG TERM SEQUELAE
sequelae

1. Infertility :
▫ Most common complication
▫ 20% of them.
cause : peritubal and periovarian adhesions
tubal blockade.
❖ Risk of infertility depends on number of episodes of
acute PID, severity and causal organism
2. Ectopic pregnancy :
▫ 6-10 fold increased risk
▫ 50% of cases with ectopic have a prev h/o PID
cause : tubal blockade & impaired ovum transport
through the tube

3. Chronic pelvic pain :
▫ 4 times increased following acute PID
cause : Hydrosalpinx and adhesions (chronic
PID)
4. Recurrent PID

CHRONIC PID
HISTORY of PREVIOUS PID clinches the
diagnosis.
C/Fs
Mostly asymptomatic
If symptomatic
☞Constant pain in lower abdomen; worse 1wk
before menstruation.
☞Low backache
☞Deep dyspareunia
☞polymenorrhagia/menorrhagia
☞Congestive dysmenorrhea
☞Vaginal discharge
☞Rectal and bladder irritation

Signs :
P/A
Tenderness in both iliac fossa
Irregular mass may be felt
P/S
Congested cervix
Mucoid/muco-purulent discharge is usually present
B/E
Uterus-retroverted and fixed
Adnexa-enlarged,thickened,tender,nodular,may be
fixed.
P/R
Thickened,fibrosed parametrium
Thick,nodular uterosacrals

D/D
1. Ectopic pregnancy
2. Uterine fibroids
3. Endometriosis
4. Ovarian tumor
5. TB tomass
Investigations
SAME AS ACUTE PID

MANAGEMENT
Most often surgical:-
Indications:
1. Severe,persistent,progressive pelvic pain
2. Severe dyspareunia due to chronic PID
3. Progressive enlargement of the tubo-ovarian
mass
4. Repeated exacerbations requiring multiple
hospitalisations
5. Ureteric obstruction resulting from ligneous
cellulitis

IDEAL SURGERY
TAH + BSO
BUT……….

CONSIDERATIONS
Age
Parity & desire for fertility
symptamatology
pelvic pathology
**Nature of surgery can be decided usually with
“abdomen open”

Young woman desirous of fertility
Conservative surgeries (when the disease is limited)
U/L Salpingectomy
U/L Salpingo-oophorectomy

SALPINGECTOMY
Incision : transverse maylard incision
Abdominal wall opened in layers
adhesions released

Kelly calmp placed on mesosalpinx beneath
fimbrial end
Mesosalpinx clamped and cut as close to the
tube as possible.

Tube excised at the uterine cornu in wedge shaped
manner
Uterine wound closed with a figure of 8(2-0) suture
Vessels in the mesosalpinx are ligated by transfixion

Peritonisation of cornual wound
-round ligament and broad ligament are brought
onto cornual wound and secured with mattress
sutures

SALPINGO-OOPHORECTOMY
adhesions released
INFUNDIBULO PELVIC ligament
identified,doubly clamped,
cut and ligated

Tubal and ovarian attachment to broad ligament
clamped and cut
Cornual end and ovarian ligament excised followed by
peritonisation

PIDAND INFERTILITY
Mild PID :
▫ Laparoscopic salpingo-ovariolysis following
establishment of tubal patency.
Tubal blockade :
▫ laparoscopic salpingoscopy and hysteroscopic
falloposcopy done followed by tuboplasty.
U/L tubal damage with opposite adnexa relatively
normal :
▫ U/L salpingectomy/salpingo-oophorectomy
*In woman with IVF as the option for future fertility,
Hydrosalpinx if present should be removed,else there will be
decreased endometrial receptivity.

188
• RCOG’s guidelines on PID and its
management are the same as mentioned in
the previous slides.
• But we would like to emphasise on specific
guidelines by RCOG to reinforce their
importance

SPECIAL NOTE ON RCOG
GUIDELINES
A detailed explanation of their conditin should be provided to
women,with particular emphasis on the longterm implications for
their health and the health of their partner.
When giving information to patients,the clinician should consider the
following:
-an explanation of what treatment is being given and its possible
adverse effects
-that following treatment fertility is usually maintained but there
remains a risk of future infertility,chronic pelvic pain or ectopic
pregnancy
-repeat episodes of PID are associated with an exponenential increase
in the risk of infertility
-future use of barrier contraception will significantly reduce the risk of
PID

-the need to screen her sexual contacts for infection to prevent her
becoming reinfected
-clinically more severe disease is associated with a greater risk of
sequelae
-the earlier treatment is given the lower the risk of future fertility
problems

INTRODUCTION
● TB was recognized as a clinical entity as far
back as 1000 BC.
● First authentic description of genital TB was by Morgagni in
1744 , who found uterus and tubes filled with caseous
material in autopsy of a 20 yr old female who died of
tuberculosis
● The word tuberculosis was first used in 1834, Robert Koch
discovered the tubercle bacilli in 1882
● it is a frequent cause of chronic PID and infertility
in developing world

INCIDENCE
● Actual incidence of pelvic tuberculosis is difficult to asses as
patients are asymptomatic
● Disease often comes to light only incidentally during the course of
investigation for a gynaecological complaint
● Genital TB responsible for- 1% of all gynaecological admissions in
India
● 5-13% cases of pulmonary Tb will develop genital Tb

➢ In infertility patients incidence 3- 16%
➢ female genital tuberculosis - disease of young
women(20-40yrs) 80%
➢ Less common in post menopausal women – Atrophic
endometrium offers poor milieu for growth of bacillus

ORGAN INVOLVEMENT IN GENITAL TB 
FALLOPIAN TUBES 90 – 100
%
ENDOMETRIUM 50 – 60
%
OVARIES 20 – 30
%
CERVIX 5 – 15 %
VULVA AND VAGINA < 1 %

• fallopian tubes(100% & bilateral)
Earliest lesion with propensity for
transluminal spread to ovary and endometrium thus
playing a central role in initiation and dissemination of
pelvic tuberculosis
• Endometrial lesions
are typically immature&frequently focal
since they shed monthly
endometrium is regularly reinfected from
tubes or basal layer of endometrium which is not shed

CLINICAL FEATURES
● The clinical diagnosis of genital TB requires a high
index of suspicion.
● Genital TB may be asymptomatic and the majority of
women are diagnosed during investigations for infertility
● 20% of patients give a history of TB in their immediate
family.
● A history of primary infertility in a woman in whom
examination reveals no apparent cause should rise
suspicion of genital Tb
●Asymptomatic (10%)

Infertility
● In 35 to 60 % of cases it may be only complaint
● Of these 75% present with primary infertility and 25% with
secondary infertility
Infertility is attributed to
Tubal factors( blocked &damaged tubes)
Endometrial factors (non-reception& damaged
endometriun with Ashermans syndrome)
Ovarian factors( poor ovarian reserve &volume)

Menstrual irregularities
Occurs in 10 to 40% of cases
● Menorrhagia
● Pubertal menorrhagia
● Dysmenorrhoea
● Hypomenorrhoea
● Amenorrhoea
● Metrorrhagia
● Postmenopausal bleeding(rarely)
Tuberculosis should be suspected if pubertal menorrhagia does not respond to medical treatment
Tuberculosis should be suspected if pubertal menorrhagia does not respond to medical treatment

●Abdominal pain/lump/ chronic pelvic
pain-
Not usually a severe pain
Episodes of acute lower abdominal pain owing to
secondary infection by pyogenic organisms may occur
• Postcoital bleeding
• Vaginal discharge
• Dyspareunia
● Systemic - Weight loss, Fatigue,Low-grade fever
 
.

PHYSICAL SIGNS
● 35–50% of patients have an entirely
normal examination.
● Abdominal mass
● Pelvic mass
• Adnexal mass(tubo-ovarian)
• Abdominal tenderness

PHYSICAL SIGNS….
●Pelvic/adnexal tenderness
Tuberculous tubo ovarian masses are less tender than
those due to pyogenic infection,
Secondary infection and acute exacerbation may
produce sharp pain and tenderness
●   Ascites
Excessive vaginal discharge
  Ulcer in the vulva, vagina, and cervix
  Enlarged uterus with pyometra
  Fistula(usually following surgical intervention)

ABDOMINAL MASS
● History of assosiated menstrual disturbances
accompanying the presence of fixed abdomino pelvic
mass should raise the suspicion of genital tuberculosis
● Tuberculous masses can be the result of tuberculous
peritonitis with matting of the omentum, mesentery, and
bowel
● Doughy feel on palpation is suggestive of tuberculous
peritonitis
● Virgin girl presenting with pelvic inflammatory mass is
almost always of tuberculous origin

Unexplained infertility/amenorrhoea
Recurrent episodes of pelvic
infections,not
responding with usual course of
antibiotics
Pelvic mass with nodules in pod

INVESTIGATIONS
Aims of investigations…
● To identify primary lesion To confirm secondary lesion
Blood(lymphocytosis, raised ESR (non-specific)
Mantoux test … (sensitivity - 55% specificity -80%)
CXR
➢A negative chest radiograph does not rule out the diagnosis
because most pulmonary lesions are arrested by the time the
genital tract becomes involved in the disease process.
➢ Active pulmonary TB in association with genital TB is rare

ENDOMETRIAL CURETTAGE
Endometrial biopsy FIRST diagnostic step
● Endometrium is the most accessible tissue for study
with a high frequency of involvement.
● Demonstration of tuberculous endometritis may be
assumed to indicate tuberculous salpingitis in
practically 100% of cases
● Negative biopsy does not exclude FGTB as
endometrium is involved only in 50-60%cases

• Obtained by D&C/hysteroscopy directed biopsy
Done a week preceeding menstruation tubercles are
present in superficial layers of endometrium & shed
during menstuation

• Material sent in 2 samples
Formalin Normal saline
Granulomas AFB staining,
Culture –BACTEC (80-90%
sensitivity) in 5-10 days
LJ (30-35% sensitivity)
results in 3 -8wks
PCR inoculation

PCR
• Rapid sensitive & specific method
• Results obtained in 24hrs
• Sample- Endometrium, menstrual blood
• Sensitivity85-90%
• false neg in 8% &false positive in 2-3%
➢ number of organisms /ml required for test to be
positive
● microscopy-10,000
● culture- 100
● pcr -10

Limitations of PCR
Cannot differentiate live & dead bacilli 
 
False +ve rate high (can pick up even single
bacteria)
Cannot differentiate infection from disease as most of
Indians may show positive PCR without suffering from
disease
 
NOT TO START ATT JUST ON +VE PCR unless there is some
other evidence of FGTB

IFN-γ RELEASE ASSAY (QUANTIFERON
GOLD)
• New class of in vitro assay that measures interferon
released by sensitized T cells after stimulation by M.
tuberculosis antigens.
• IGRAs cannot distinguish between latent infection
and active tuberculosis (TB) disease,
• A positive IGRA result may not necessarily indicate
active TB
• However, a negative IGRA result rules out the
possibility of both active and latent tuberculosis.

Advantages • Requires a single patient visit to draw a blood
sample.
• Results can be available within 24 hours.
• Does not boost responses measured by
subsequent tests, which can happen with
tuberculin skin tests (TST).
• Is not subject to reader bias that can occur with
TST. Is not affected by prior BCG vaccination.

limitations
✓ Blood samples must be processed within 12 hours after
collection while white blood cells are still viable
✓ There is limited data on the use of QFT-G in children
younger than 17 years of age, persons recently exposed to
M. tuberculosis, and in immunocompromised persons
✓ Errors in collecting or transporting blood specimens or in
running and interpreting the assay can decrease the
accuracy of QFT-
✓ False positive results can occur with other species

IMAGING-(HSG,USG,CT,MRI)
✓ Imaging changes are observed late in the disease
✓ No characteristic radiographic features are
pathognomonic for genital tract TB(NON-SPECIFIC)
✓ Certain findings should raise suspicion of its possibility because
the diagnosis is based on the presence of calcification , strictures,
which are associated with a long list of differential diagnosis
✓ Diagnosis is not established based on imaging

➢ loculated ascites
➢ bilateral predominantly solid, adnexal
massescontaining scattered small calcification
➢ thickened omentum
➢ thickened peritoneum
➢ endometrial involvement

Ascites with lattice network of fibrin
bands
Echogenic dense and fine particulate
ascites

Ultrasound picture
showing bright
(hyperechoic) uterine
lining - scar tissue in
uterine cavity

: A classical tubo-ovarian mass consists of a fluid ovary
surrounded by a fluid filled tube. Scan shows a lobulated
fluid lesion in the ovary draped by a hydrosalpinx which
is thin-walled and clear.

3D rendering reveals a
variably echogenic ovary
surrounded by a
multilocular hydrosalpinx.

HSG

● HSG is contraindicated in proven cases of TB
as risk of reactivation
● Features….

Tobacco pouch
hydrosalpinx &
pyosalpinx
A rigid non peristalitic pipe like
tube
lead pipe

In 25–50% of cases of genital TB
the tubes remain patent with
recognizable everted fimbriae,
even if the remaining tube is
enlarged and distended, the so-
called “tobacco-pouch
appearance.”

Beaded tube .
Multiple constrictions along
the fallopian tube
Calcification of
tube

Cobblestone appearance 
 
Intraluminal scarring of the tube
radiographic sign of intraluminal adhesions

Multiple rounded filling
defects following
intraluminal granuloma
formations within the
hydrosalpinx, resembling a
" leopard skin"
appearance .
➢Bilateral cornual
block with absence
of spillage into
cavity

Vertically fixed tubes secondary
to dense peritubal adhesions. The
hyperconvulated is seen in right
tube and manifests a 
" cork screw" like appearance
" Golf club" tube.
Sacculation of both tubes in
distal portion with an
associated hydrosalpinx

-+
Peritubal halo
Thickening of the tubal
walls due to peritubal
adhesions represents a
cloudy sign .
vascular or
lymphatic
Extravasation

UTERINE CHANGES IN HSG 
➢ Small uterine cavity with
irregular contour and resembling
septate appearance
➢ Complete obstruction of uterine
cavity with glove’s finger
appearance. Pelvic calcification
{NETTER SYNDROME]

Unilateral obliteration followed by unilateral
scar in uterine cavity and revealed pseudo
unicornuate appearance 
Filling
defects

HYSTEROSCOPY
1. Small uterine cavity
2. Intra uterine adhesions
3. Scanty Endometrium
4. Tubercles
5. Endometrial calcifications
6. Absent Ostia
7. Peri osteal fibrosis
8. Caseous material coming from
OStia

View of the inside of a scarred uterine cavity using hysteroscopy
________________________________________________________________
 
Thick white scar tissue is
seen 
White patches are the
scarred areas of
adhesions, pink is normal
tissue, dark red is blood

scarring of endometrium 
Area of left tubal opening at 3
o'clock 
Area of right tubal opening at 9
o'clock 
Scarred region is in the middle

LAPROSCOPY(FROZEN PELVIS)
1. absence of endometrial evidence
2. tubercles on peritoneum /ovary/
tubes
3. tubovarian masses
4. caseous nodules
5. encysted ascitis
6. pelvic adhesions
7. normal looking tubes
8. hydrosalpinx & pyosalphinx

DIFFERENTIAL DIAGNOSIS
TUBO OVARIAN MASS
Due to other organisms
Ectopic pregnancy
Pelvic endometriosis( chocolate cyst)
Ovarian cyst
AMENORRHOEA
Pregnancy
ectopic

MANAGEMENT
Once diagnosed a gynecologist must consider
following points:-
Rule out active T.B. at any other site.
Know the extent of genital lesion.
Will medical management cure the lesion?
Is pregnancy possible following treatment?

CHEMOTHERAPY
● The first line of treatment is with anti tuberculous drugs
● All drugs can be given daily/ intermittently(3 times a week)
● Under DOTS strategy TB classified as CATEGORY 1(severe
extrapulmonary tb)
Treatment given in 2 phases
➢INITIATION PHASE-majority of bacilli are killed symptoms
resolve ,pt. becomes non-infectious
➢CONTINUATION PHASE-eliminates persisting bacteria
prevents relapse

•  
 
 
 
 
 
FIRST LINE DRUGS- 
ISONIAZID 
RIFAMPICIN 
PYRAZINAMIDE 
ETHAMBUTOL 
cat 1- 2(HRZE) +4(HR) 
cat 2-(relapse/failure cases) 
2(HRZES)+1(HRZE)+5(HRE)

SECOND LINE DRUGS- 
capreomycin 
amikacin 
kanamycin 
para amino salicylic acid 
flouroquinolones(ciprofloxacin,ofloxacin,levoflox
acin) 
ethionamide 
cycloserine

DRUG Daily oral
dose
Nature Toxicity Comments
Isoniazid 5mg/kg
Max-300mg
Bactericidal Hepatitis,peri
pheral
neuropathy
Check LFT,
Combine
pyridoxine
50mg daily
Rifampicin 10mg/kg
Max-600mg
Bactericidal Hepatic
dysfunction,
Orange
discolouration
urine,febrile
avoid- ocp
Monitor liver
enzymes
Pyrizinamide 20-25mg/kg
Max-2gm
Bactericidal Hepatitis,hype
ruricaemia,GI
upset,arthralgi
a
LFT,
Active against
intracellular
dividing forms
Ethambutol 15-20mg/kg
Max-2.5gm
Bacteriostatic Visual
disturbances,o
ptic
neuritis,loss of
Ophthalmosco
pic prior to
therapy

● all hiv infected TB patients are candidates
for ART 
wen to start ART??
Within first 8 weeks of anti tb treatment
● RIFAMPICIN IN HIV?
Rifampicin potent inducer of cyt p450
enzymes lowers serum levels of PI&NNRTIS
Rifabutin-much less enzyme inducer used 
HIV-associated TB

SURGERY
surgery should be preceeded by several weeks of
chemotherapy and followed by full course of chemotherapy
INDICATIONS-
● Unresponsiveness of active disease in spite of adequate anti-
tubercular tx
● Tubercular pyosalphinx
● Ovarian abscess
● Pyometra
● Persistent menorrhagia,chr pelvic pain causing deteriorating
health status

CONTRAINDICATIONS
● Presence of active tb in extragenital region
● Favourable respose with dec in mass size
● Accidental discovery of tubercular tubo ovarian mass
on laprotomy in young pt.-abdomen is closed after
taking tissue for biopsy
● Extensive bowel adhesions(fistula formation)

Types of surgery- 
● Removal of adnexal mass in young woman
● Drainage of pyometra
● Fistula repair
● Imaging guided interventions in the treatment:
● Fluoroscopy guided recanalization of cornual block.
● USG guided drainage of tubo-ovarian collections.
Tuboplasty-CI
Any treatment on tube will reactivate disease
Fertility cannot be restored when tubal walls are damaged

Follow up
● Pt needs to be followed up for atleast 5 yrs as
reactivation of the lesion has been reported during
this period
● Yrly or when indicated curettage should be carried
out to check for any reactivation
patient must be considered cured if –
At least 2 reports including histological and
bacteriological examination becomes negative

PROGNOSIS
● 90%-cured
● only 10%-fertility restored
● Of these who conceived 50% -tubal pregnancy
● 20-30%-abort
● Only 2%-live births

INVITRO FERTILIZATION- 
Women successfully treated for genital Tb are offered
assisted reproduction by IVF
40%-success provided endometrium normal
In cases of endometrial damage(sorrogacy or adoption)

Pelvic inflammatory disease 2

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