• PID is the most common serious infection in young women of reproductive age (15–44 years).
• Estimated incidence: approximately 1–2% per year among sexually active young women.
• In Hong Kong, Chlamydia trachomatis and Neisseria gonorrhoeae remain the most important sexually transmitted causes, though the exact prevalence is likely underestimated due to subclinical cases ^[1][3].
• Up to 60–70% of PID cases may be subclinical ("silent PID") — the patient never presents acutely but develops sequelae (tubal factor infertility, ectopic pregnancy) years later.

• Peak age: 15–25 years (coincides with peak sexual activity and higher biological susceptibility of the adolescent cervix — the adolescent cervix has a larger ectropion/ectopy zone with more columnar epithelium exposed, which is the preferred target for Chlamydia and Gonorrhoea).
• Rare before menarche (no ascending route without menstruation/cervical mucus changes) and after menopause (cervical mucus plug is more protective; lower sexual activity).

Protective factors:

• Barrier contraception (condoms) — physical barrier against STIs
• Combined oral contraceptive pills (COCPs) — thicken cervical mucus (progestogen effect) → harder for organisms to ascend; also reduce menstrual flow (less retrograde menstruation to carry organisms). However, COCPs may mask symptoms of PID (lighter periods, less pain) and may encourage not using condoms, so the epidemiological picture is complex.

Cervix:

• Acts as the gatekeeper between the lower and upper genital tracts.
• The cervical mucus plug is a physical and immunological barrier (contains IgA, lysozyme, lactoferrin).
• During menstruation, the cervical os opens slightly and the mucus plug thins → this is why PID often starts during or just after menstruation.
• Cervical ectopy (columnar epithelium on the ectocervix) — particularly extensive in adolescents and COCP users — provides a large target for Chlamydia which preferentially infects columnar epithelial cells.

Endometrium:

• When organisms ascend past the cervix, they first cause endometritis.
• The endometrium is shed monthly (menstruation), which is partly protective — but during infection, the shedding endometrium can actually facilitate spread by exposing raw surfaces.

Fallopian Tubes (Salpinges):

• These are the most vulnerable and most important structures in PID.
• The tubal mucosa is lined with ciliated columnar epithelium — these cilia beat in a coordinated wave to transport the ovum from ovary to uterus.
• Inflammation (salpingitis) causes:
  • Destruction of cilia → impaired ovum transport → ectopic pregnancy or infertility
  • Mucosal adhesions → tubal occlusion → infertility
  • Pyosalpinx (pus-filled tube) → if the fimbriated end seals shut and tube fills with pus
  • Hydrosalpinx (fluid-filled tube) → chronic sequel after the acute infection resolves but the tube remains blocked and fills with serous fluid
• The fimbriae (finger-like projections at the distal end) are especially delicate and easily damaged.

Ovaries:

• Usually involved secondarily (tubo-ovarian abscess = TOA).
• Ovarian tissue is relatively resistant to infection due to its thick tunica albuginea, but if the surface is breached (e.g., at ovulation when the follicle ruptures), bacteria can enter.

Pelvic Peritoneum:

• The fallopian tubes open directly into the peritoneal cavity (they are NOT closed tubes — the abdominal cavity in females communicates with the outside world via the tubes → uterus → cervix → vagina).
• This is why organisms can spread to cause pelvic peritonitis and even reach the liver capsule (perihepatitis / Fitz-Hugh-Curtis syndrome).

Pouch of Douglas (Rectouterine Pouch):

• The most dependent part of the peritoneal cavity in the upright position.
• Pus collects here → pelvic abscess / pouch of Douglas abscess.
• Can be detected on bimanual exam (fullness/tenderness in the posterior fornix) or on ultrasound.

These are the organisms that initiate the ascending infection by first causing cervicitis, then ascending.

Once the STI organisms have breached the cervical barrier and initiated inflammation, the damaged mucosa allows normal vaginal commensals (which are normally kept in check) to ascend and contribute to the polymicrobial infection:

• Actinomyces israelii — associated with long-term IUD use (particularly the older copper IUDs). Causes a chronic, indolent granulomatous infection. Think of this if a woman has had an IUD in situ for years and develops a pelvic mass.
• Mycobacterium tuberculosis — genital TB is an important cause of PID in endemic areas including Hong Kong, particularly among immigrants from mainland China and Southeast Asia ^[4]. Causes chronic granulomatous salpingitis → Asherman syndrome (intrauterine adhesions), tubal occlusion, infertility. Often presents as infertility rather than acute PID.

1. STI organisms (Chlamydia or Gonorrhoea) are sexually transmitted and colonise the endocervical columnar epithelium.
2. Chlamydia trachomatis is an obligate intracellular pathogen — it enters the epithelial cell, replicates within inclusion bodies, then lyses the cell to spread. This intracellular lifestyle explains:
   • Why it is often asymptomatic (evades extracellular immune detection)
   • Why it causes a relatively indolent, chronic inflammatory response
   • Why cell-mediated immunity (not antibodies) is the key host defence
3. Neisseria gonorrhoeae attaches to columnar epithelium via pili and Opa proteins, invades transmurally, and elicits a vigorous neutrophilic response → purulent exudate (the classic purulent discharge of gonorrhoea).

Organisms ascend from cervix → endometrium → fallopian tubes via several mechanisms:

• Passive transport: organisms carried upward by menstrual reflux, uterine contractions, or the negative pressure created by cervical dilation during menstruation.
• Active transport: some organisms (especially gonococci) can actively migrate through mucus. Trichomonas vaginalis (if co-present) can act as a "Trojan horse" — carrying bacteria on its surface and facilitating their ascent.
• Sperm as vectors: spermatozoa can carry bacteria attached to their surface from the lower to the upper genital tract.
• Instrumentation: IUD insertion, D&C, or other procedures can physically introduce organisms.

Why does ascending infection occur more easily during menstruation?

• Cervical mucus plug is thinnest
• Cervical os is slightly dilated
• Menstrual blood provides a culture medium (rich in iron and nutrients)
• Loss of the endometrial barrier exposes raw surfaces
• Retrograde menstrual flow can carry organisms into the tubes

• Organisms infect the endometrium → endometritis.
• Clinically: intermenstrual bleeding (IMB), menorrhagia, dysmenorrhoea.
• Histologically: plasma cells in the endometrial stroma (the hallmark of chronic endometritis).
• The endometrium is somewhat resistant because it is shed monthly, so endometritis alone is often transient — but it represents the gateway to the tubes.

This is where the real damage occurs:

1. Organisms reach the fallopian tube mucosa (endosalpinx).

2. The delicate ciliated columnar epithelium of the tube is infected → intense inflammatory response.

3. Acute salpingitis: neutrophilic infiltration, mucosal oedema, exudate (purulent material within the tubal lumen).

4. The inflammation causes:

   • Deciliation — loss of ciliated cells → impaired ovum transport
   • Mucosal plication fusion — the folds of the tubal mucosa stick together
   • Tubal wall oedema and thickening → narrowing of the lumen
   • Fimbrial agglutination — the delicate fimbriae stick together and the distal end of the tube seals shut

5. If the fimbriated end seals → pyosalpinx (pus trapped in a sealed tube) → can progress to tubo-ovarian abscess (TOA) if the ovary is also involved (especially if ovulation has occurred, creating a breach in the ovarian surface).

• Since the tubes open into the peritoneal cavity, organisms and purulent exudate spill into the pelvis → pelvic peritonitis.
• Pus collects in the Pouch of Douglas (most dependent part).
• Organisms can track along the right paracolic gutter (the natural anatomical channel along the right side of the abdomen) to reach the liver capsule → Fitz-Hugh-Curtis syndrome (perihepatitis) ^[2][3].

Fitz-Hugh-Curtis syndrome is a rare complication of pelvic inflammatory disease involving liver capsule inflammation leading to the formation of adhesions presenting with the clinical syndrome of right upper quadrant pain. ^[2]

• On laparoscopy, this produces the classic "violin string" adhesions between the liver capsule (Glisson's capsule) and the anterior abdominal wall / diaphragm ^[3].
• The liver parenchyma itself is NOT infected — it is purely perihepatitis (inflammation of the peritoneum covering the liver).

A critical concept: much of the tubal damage in chlamydial PID is caused not by the organism itself, but by the host immune response:

• Chlamydia trachomatis produces chlamydial heat shock protein 60 (cHSP60).
• cHSP60 shares molecular mimicry with human HSP60 (found on tubal epithelial cells).
• The immune response against cHSP60 cross-reacts with the host's own tubal epithelium → autoimmune-mediated tubal destruction.
• This is why repeated chlamydial infections cause exponentially worse tubal damage — each re-infection amplifies the autoimmune response (anamnestic immune response).
• This also explains why subclinical/silent chlamydial PID can cause severe tubal damage despite minimal symptoms — the immune-mediated damage is occurring silently.

• Absence of fever does NOT exclude PID — most patients with mild-moderate PID are afebrile.
• Absence of discharge does NOT exclude PID — some patients (especially Chlamydia) have minimal discharge.
• Normal inflammatory markers do NOT exclude PID — sensitivity of CRP/ESR/WCC for PID is only ~60–70%.
• Negative STI tests do NOT exclude PID — remember, PID is polymicrobial; STI organisms are found in only ~30–50% of cases (vaginal anaerobes may be the predominant organisms).

Up to 60-70% of PID (particularly chlamydial PID) is subclinical:

• The patient has no acute symptoms or only vague, mild symptoms that are attributed to "period pain" or dismissed.
• The diagnosis is only made retrospectively when the patient presents with:
  • Tubal factor infertility (HSG or laparoscopy shows tubal occlusion)
  • Ectopic pregnancy (damaged tube fails to transport the embryo)
  • Chronic pelvic pain (adhesions from prior silent inflammation)
• This is why screening for Chlamydia in high-risk populations is a public health priority.

• PID in the first trimester can present similarly to ectopic pregnancy or threatened miscarriage.
• Obstetric complications of PID/STIs include: ectopic pregnancy, prematurity, premature rupture of membranes, chorioamnionitis, septic abortion, and post-abortal PID. ^[3]
• PID is rare in established pregnancy (the mucus plug and decidual reaction provide protection), but endometritis can occur post-partum or post-abortion.

• As noted above, risk is only in the first 3 weeks post-insertion.
• If mild-moderate PID develops in a woman with an IUD, the IUD does NOT need to be removed initially — start antibiotics and reassess at 48–72 hours.
• If no improvement at 48–72 hours, consider IUD removal.
• Actinomyces israelii should be considered in women with long-standing IUDs who develop chronic PID or a pelvic mass.

The lecture notes highlight important causes of treatment failure:

• Ping-pong infection (re-infection from untreated partner)
• Treatment failure (e.g., non-compliance)
• Infections other than Chlamydia trachomatis: e.g., Mycoplasma genitalium, Ureaplasma urealyticum, HSV, Trichomonas vaginalis ^[3]
• Prostatic disease (in male partners — chronic prostatitis harbouring organisms) ^[3]

Teaching point from senior notes ^[5]: "PID: lower abdominal pain (lower than appendicitis), usually bilateral and exacerbated by coitus (dyspareunia). A/w vaginal discharge, dysmenorrhea and dysuria. P/E shows diffuse lower abd tenderness, purulent endocervical D/C, cervical excitation and adnexal tenderness." — This comparison is directly contrasting PID against appendicitis and is very high-yield for exams.

When PID causes Fitz-Hugh-Curtis syndrome, the patient may present with RUQ pain that mimics:

• Acute cholecystitis (RUQ pain, Murphy's sign, fever)
• Hepatitis (RUQ tenderness, jaundice)
• Right basal pneumonia (referred RUQ pain, pleuritic)

How to differentiate: Fitz-Hugh-Curtis occurs in a young, sexually active woman with concurrent or recent lower pelvic symptoms. LFTs are usually normal (liver parenchyma is unaffected). USG shows no gallstones and a normal gallbladder. If laparoscopy is performed, "violin string" adhesions are seen between the liver capsule and anterior abdominal wall ^[8].

When considering pelvic mass as a differential, classify by gynaecological vs. non-gynaecological (gastrointestinal, urologic, retroperitoneal). Don't forget about pregnancy — especially for teenage girls. Also consider pseudocyst related to previous surgeries. ^[9]

A TOA (tubo-ovarian abscess) presents as a pelvic mass and must be differentiated from:

• Ovarian neoplasm (benign or malignant)
• Endometrioma
• Ectopic pregnancy
• Fibroid
• Pelvic kidney
• Diverticular abscess
• Appendicular abscess

Presumptive diagnosis of PID: Sexually active women experiencing pelvic or lower abdominal pain, in the absence of other cause, with either cervical motion or uterine or adnexal tenderness. ^[1][2]

Let's break this down — there are three components, ALL of which must be present:

The minimum criteria above are highly sensitive but not very specific (PPV is only ~65–90%). The following additional findings increase the likelihood of PID and should be sought:

These are used primarily in research or when the diagnosis is uncertain:

Hysterosalpingogram (HSG) carries a 4–5% risk of causing PID ^[13]. This is because the procedure involves injecting contrast through the cervix into the uterine cavity and fallopian tubes — if there are subclinical organisms in the cervix, the procedure can push them into the upper genital tract. This is why:

• Some centres screen for Chlamydia before HSG (and treat if positive)
• Some give prophylactic antibiotics before HSG
• HSG is absolutely contraindicated in active PID

HSG also has limitations: false positive results can occur due to spasm in proximal tubal ends (mimicking tubal occlusion), and peritubal adhesions cannot be detected ^[13] — contrast may spill into the peritoneal cavity normally even if adhesions are present around the tube externally.

When a pelvic mass is discovered on investigation, it should be classified as gynaecological vs. non-gynaecological (gastrointestinal, urologic, retroperitoneal). Don't forget pregnancy, especially in teenage girls, and pseudocysts related to previous surgeries. ^[14]

In PID, the pelvic mass is usually a TOA — but the differential for a pelvic mass on imaging includes ovarian neoplasm, endometrioma, ectopic pregnancy, fibroid, pelvic kidney, and diverticular/appendicular abscess. Correlation with clinical context and tumour markers (CA-125, AFP, βhCG, LDH) may be needed.

The lecture slides explicitly list the indications for inpatient treatment: ^[16]

Intravenous antibiotic should be continued until 24 hours after clinical improvement and followed by oral therapy. ^[16]

If NONE of the above indications are present, the patient can be managed as an outpatient with:

• Oral antibiotics
• Clear instructions for follow-up at 48–72 hours
• Advice on rest, analgesia, abstinence from intercourse until treatment is complete
• Partner treatment arranged

UK BASHH 2018 / CDC 2021 / QMH Guidelines — Recommended Outpatient Regimen:

So the outpatient regimen in summary:

IM Ceftriaxone (single dose) + Oral Doxycycline (100 mg BD × 14 days) + Oral Metronidazole (400 mg BD × 14 days)

Alternative outpatient regimen (if ceftriaxone not available):

Recommended IV Regimen:

Alternative IV Regimen:

This regimen is particularly useful for TOA because clindamycin penetrates abscess cavities exceptionally well (unlike many beta-lactams which are inactivated at the low pH found in abscesses).

IV antibiotics should be continued until 24 hours after clinical improvement, then switched to oral therapy ^[16]:

• Oral step-down: Doxycycline 100 mg BD + Metronidazole 400 mg BD to complete a total of 14 days.

Treatment failure (no improvement at 48–72 hours):

The lecture slides and senior notes emphasise causes of symptom persistence despite treatment: ^[8]

• Ping-pong infection — partner not treated → re-infection
• Treatment failure / non-compliance — patient not taking medications correctly
• Infections other than Chlamydia trachomatis — M. genitalium, Ureaplasma urealyticum, HSV, Trichomonas vaginalis ^[8]
• Prostatic disease in male partner (chronic prostatitis harbouring organisms) ^[8]

Management of treatment failure:

1. Reassess the diagnosis (is it really PID? Consider imaging to look for TOA, appendicitis, etc.)
2. Check compliance
3. Ensure partner has been treated
4. Consider M. genitalium — test with NAAT if available; treat with azithromycin 1g stat followed by 250 mg/day × 4 days or moxifloxacin 400 mg/day × 10–14 days ^[8] (moxifloxacin has the best activity against macrolide-resistant M. genitalium)
5. Consider Trichomonas vaginalis — treat with metronidazole 400 mg BD × 5–7 days ^[8]
6. Escalate to IV antibiotics if on oral therapy
7. Consider laparoscopy for diagnostic and therapeutic purposes

IUD management in PID:

• Mild–moderate PID with IUD in situ: do NOT remove the IUD immediately. Start antibiotics and reassess at 48–72 hours.
• If no improvement at 48–72 hours despite adequate antibiotics: remove the IUD (it may be acting as a nidus for biofilm).
• Send the removed IUD tip for culture (including Actinomyces if long-standing IUD).

What it is: A walled-off collection of pus involving the fallopian tube and ovary, often forming a complex inflammatory mass. It represents the most serious acute complication of PID.

Pathophysiology:

• Acute salpingitis → purulent exudate fills the tubal lumen → the fimbriated end seals shut (fimbrial agglutination) → pyosalpinx (pus-filled sealed tube).
• If ovulation has recently occurred, the ovarian surface has a breach (the ovulation stigma) through which bacteria can enter the ovarian parenchyma.
• The inflamed tube adheres to the ovary, and the pyosalpinx extends into the ovarian tissue → a combined tubo-ovarian abscess forms.
• The abscess cavity is predominantly anaerobic (oxygen is consumed by the intense inflammatory process), which is why anaerobes (Bacteroides, Prevotella) thrive and why metronidazole is essential in treatment.

Clinical features:

• Swinging/spiking fever (hectic fever pattern — classic of abscess: the body temperature swings widely as the abscess intermittently releases bacteria/toxins into the bloodstream)
• Severe pelvic pain, often with peritoneal signs
• Palpable adnexal mass on bimanual examination (tender, boggy, fixed)
• Markedly elevated WCC, CRP
• TVS: complex adnexal mass with thick walls, internal echoes, septations, ± fluid-fluid levels

Management (from the senior notes) ^[17]:

75% of TOA will respond to antibiotics alone ^[17]. Antibiotic treatment is appropriate if:

• No signs/symptoms of rupture of TOA: i.e., no acute abdomen, vitals stable
• Abscess < 7 cm in diameter
• Responding to IV antibiotic therapy

Surgical drainage is indicated if ^[17]:

• Sepsis ± ruptured TOA
• Large abscess ≥ 7 cm in diameter not responding to antibiotic treatment
• No response to IV antibiotics in 48–72 hours, as characterised by:
  • Clinical: persistent/new onset fever, abdominal pain, enlarging pelvic mass
  • Biochemical: persistent elevated WCC, sepsis

Surgical options: ± salpingotomy/salpingectomy, unilateral salpingo-oophorectomy (USO), total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAHBSO) ^[17] — the extent of surgery depends on the degree of tissue destruction, the patient's age, and her desire for future fertility. Fertility-sparing surgery (drainage alone, or unilateral salpingectomy) is preferred in young women whenever possible.

Ruptured TOA:

• This is a life-threatening surgical emergency.
• The walled-off abscess ruptures into the peritoneal cavity → generalised purulent peritonitis → septic shock.
• Presents with sudden worsening of pain, diffuse peritonism (rigid abdomen, guarding, absent bowel sounds), haemodynamic collapse (tachycardia, hypotension).
• Mortality: 5–10% (even with emergency surgery).
• Management: immediate resuscitation (IV fluids, broad-spectrum IV antibiotics, vasopressors if needed) + emergency laparotomy (drainage, washout, removal of necrotic tissue ± TAHBSO if tissue destruction is overwhelming).

Pathophysiology: Severe PID (especially with TOA or ruptured TOA) can lead to bacteraemia → systemic inflammatory response syndrome (SIRS) → sepsis → septic shock.

• Gram-negative organisms (e.g., E. coli, Bacteroides) release endotoxin (lipopolysaccharide/LPS) → activates the innate immune system (TLR4 on macrophages) → massive cytokine release (TNF-α, IL-1, IL-6) → vasodilation, capillary leak, myocardial depression → distributive shock.
• Requires aggressive resuscitation: the Surviving Sepsis Campaign "hour-1 bundle" (blood cultures, lactate, IV fluids, broad-spectrum antibiotics within 1 hour, vasopressors if MAP < 65 despite fluids).

Pathophysiology: Purulent material spills from the fallopian tubes (which open directly into the peritoneal cavity) → inflammation of the pelvic peritoneum. May remain localised (pelvic peritonitis) or become generalised (diffuse peritonitis) if not treated.

• Pus collects in the Pouch of Douglas (the most dependent part of the peritoneal cavity in the upright position).
• Presents with severe lower abdominal pain, peritoneal signs (guarding, rigidity, rebound tenderness), absent bowel sounds (paralytic ileus due to peritoneal inflammation inhibiting gut motility).

Fitz-Hugh-Curtis syndrome is a rare complication of pelvic inflammatory disease involving liver capsule inflammation leading to the formation of adhesions presenting with the clinical syndrome of right upper quadrant pain. ^[2][8]

Pathophysiology:

• Organisms (particularly C. trachomatis and N. gonorrhoeae) spread from the pelvis to the liver capsule via two routes:
  1. Direct peritoneal spread — organisms travel along the right paracolic gutter (the anatomical channel between the ascending colon and the right lateral abdominal wall) from the pelvis to the subhepatic/subdiaphragmatic space.
  2. Lymphatic/haematogenous spread — less common.
• The liver capsule (Glisson's capsule) and the overlying parietal peritoneum become inflamed → perihepatitis.
• The liver parenchyma itself is NOT infected — this is why LFTs are typically normal.
• As inflammation resolves, fibrinous adhesions form between the liver capsule and the anterior abdominal wall/diaphragm → the classic "violin string" adhesions seen on laparoscopy ^[8].

Clinical features:

• Right upper quadrant pain — can be severe, pleuritic (worse on inspiration), and may radiate to the right shoulder (phrenic nerve irritation from diaphragmatic peritoneal inflammation).
• May be the presenting complaint (patient may not report pelvic symptoms or they may be mild/subclinical).
• Mimics: acute cholecystitis, hepatitis, right basal pneumonia, pulmonary embolism, peptic ulcer.
• LFTs typically normal (distinguishes from hepatitis/cholangitis).
• Abdominal USS: normal gallbladder, no gallstones (distinguishes from cholecystitis).

Prevalence: Occurs in approximately 5–10% of PID cases. More common with chlamydial PID.

Recurrent PID: 1/4 may have a further episode. ^[18]

Recurrent PID occurs in 25% of individuals. ^[17]

Why does PID recur?

1. Re-infection: The most common cause — the patient is re-exposed to STI organisms (untreated partner/new partner). Each new infection causes additional tubal damage.
2. Incomplete treatment: Non-compliance, inadequate regimen, or resistant organisms.
3. Impaired local immunity: Previous PID damages the mucosal immune defences of the upper genital tract, making it more susceptible to future infections.
4. Behavioural risk factors persist: The same risk factors (multiple partners, unprotected sex) that caused the first episode often continue.

Clinical significance: Each additional episode of PID exponentially increases the risk of tubal factor infertility (see below). This is why prevention of recurrence (partner treatment, safe sex education, STI screening) is paramount.

Chronic pelvic pain: dysmenorrhoea, dyspareunia. 15–20%. ^[17][18]

Definition: Menstrual or non-menstrual pain for ≥ 6 months occurring below the umbilicus ^[17].

Pathophysiology:

• Cause: result from scarring and adhesions from PID-associated inflammation ^[17].
• Pelvic adhesions (bands of fibrous scar tissue) bind the pelvic organs together (tubes, ovaries, uterus, bowel, omentum) → these adhesions are pulled and stretched during normal activities (walking, exercise, sexual intercourse, defecation, menstruation) → chronic visceral pain.
• Adhesions can also entrap nerve fibres, causing neuropathic pain.
• Dysmenorrhoea (painful periods) — adhesions tether the uterus, preventing normal uterine contractions during menstruation; endometritis may persist as chronic endometritis.
• Deep dyspareunia (pain during deep penetration) — the cervix is pushed against inflamed/scarred adnexal structures during intercourse.

Management: Difficult. Options include:

• Analgesia (NSAIDs, paracetamol, neuromodulators like amitriptyline/gabapentin for neuropathic component)
• Laparoscopic adhesiolysis (division of adhesions — but adhesions tend to re-form, so long-term benefit is uncertain)
• Physiotherapy, psychological support (chronic pain management multidisciplinary approach)

Subfertility (~20%): 13% after 1 episode, 36% after 2 episodes, 75% after 3 episodes. ^[17]

This is the most feared long-term consequence of PID.

Pathophysiology: Reason: loss of ciliary action, fibrosis, tubal occlusion. ^[17]

Let's trace the mechanism from first principles:

1. Acute salpingitis destroys the ciliated columnar epithelium of the tubal mucosa.
2. The denuded mucosa heals by fibrosis (replacement of specialised epithelium with non-functional scar tissue).
3. Mucosal folds (plicae) adhere to each other → intraluminal adhesions → the tubal lumen narrows or completely occludes.
4. The fimbriae (the finger-like projections that "capture" the ovum after ovulation) become agglutinated and non-functional → the tube can no longer pick up the ovum.
5. Result: tubal factor infertility — the ovum cannot reach the sperm, or the fertilised embryo cannot reach the uterus.

If the tube is completely occluded at the fimbriated end:

• Tubal secretions and transudates accumulate in the sealed tube → hydrosalpinx ("hydro" = water, "salpinx" = tube).
• Hydrosalpinx fluid is toxic to embryos — even if IVF is attempted, the hydrosalpinx fluid can leak into the uterine cavity and impair implantation. This is why salpingectomy (removal of the hydrosalpinx) is recommended before IVF in women with hydrosalpinges.

Risk factors for subfertility after PID: chlamydia infection, delay in seeking care (≥ 3 days), increased number of PID episodes, increased PID severity. ^[17]

Ectopic pregnancy (7× increased risk) ^[17]: due to tubal blockage.

The senior notes list ectopic pregnancy as a complication of both PID and gonorrhoea. ^[8]

Pathophysiology:

• PID damages the tubal mucosa → loss of cilia + partial tubal occlusion (not complete occlusion).
• Spermatozoa are small enough to navigate through a partially damaged tube to reach and fertilise the ovum.
• However, the fertilised embryo (which is much larger than a sperm) is too large to pass through the narrowed, adhesion-bound, deciliated tube back to the uterus.
• The embryo implants in the tube wall instead → tubal ectopic pregnancy.
• This is the most dangerous type of ectopic because the tube cannot accommodate a growing pregnancy → rupture → life-threatening intra-abdominal haemorrhage.

Why 7× risk?

• In the general population, ectopic pregnancy occurs in ~1–2% of pregnancies.
• After PID, this rises to ~7–10% (roughly 7× baseline) because the tubes are partially damaged in so many cases.
• Women with a history of PID should have early pregnancy ultrasound (at 6–7 weeks) to confirm intrauterine pregnancy location.