Clinical overview
Tubal infection — salpingitis — is the pathological lesion that underlies most of the clinical phenomena of pelvic inflammatory disease. Understanding the pathology explains the clinical findings: why cervical motion tenderness occurs, why some women develop tubo-ovarian abscesses while others recover completely, why infertility and ectopic pregnancy follow some episodes, and why "burnt-out" PID can leave chronic pain. The chapter walks through the temporal evolution of tubal infection from acute mucosal inflammation through chronic damage, correlating each stage with the clinical picture the registrar sees in clinic.
Core knowledge
Microbiology recap
See acute-pelvic-infection for full epidemiology. Briefly: Chlamydia trachomatis (silent ascent, gradual damage), Neisseria gonorrhoeae (more acute), Mycoplasma genitalium, anaerobes (particularly in TOA), and in South Africa, Mycobacterium tuberculosis (genital TB) — an important cause of chronic salpingitis and tubal infertility, especially in HIV-positive women.
Stages of tubal pathology
Acute salpingitis can close fimbriae, fill the tube with pus, and fuse tube and ovary into a TOA.
Acute salpingitis (early stage):
- Mucosal hyperaemia and oedema.
- Polymorphonuclear (neutrophil) infiltrate in lamina propria.
- Loss of ciliary action on columnar epithelium (early functional damage even when histology looks modest).
- Tubal lumen contains serous-to-purulent exudate.
- Clinical correlate: bilateral lower abdominal pain, deep dyspareunia, cervical motion tenderness (from inflamed broad ligament tugged by cervix), fever, raised WCC and CRP. Mucopurulent cervical discharge.
Acute salpingitis (advanced):
- Tubal wall thickened, congested.
- Pus in lumen → pyosalpinx.
- Fimbriae become oedematous, agglutinated → closure.
- Peritubal inflammation extends to involve ovary, broad ligament, pouch of Douglas.
- Clinical correlate: severe pain, more systemic features, palpable adnexal mass, peritoneal signs if inflammation reaches parietal peritoneum.
Tubo-ovarian abscess (TOA):
- Tube and ovary fused into a single inflammatory mass with central liquefactive necrosis.
- Polymicrobial — anaerobes dominate.
- Capsule of granulation tissue contains abscess; if it ruptures, generalised peritonitis follows.
- Clinical correlate: severe constant pain, high fever, marked systemic illness, complex adnexal mass on TVS, often unilateral.
Chronic salpingitis (resolution / scarring stage):
- Plasma cell infiltrate replaces neutrophils.
- Fibrosis of tubal wall.
- Adhesions between mucosal folds (forming compartments — "follicular salpingitis").
- Adhesions between tube and surrounding structures (ovary, bowel, omentum, pelvic side wall).
- Fimbrial agglutination → hydrosalpinx (distended fluid-filled tube with thin wall, watery contents).
- Clinical correlate: chronic pelvic pain, infertility, deep dyspareunia. Tubal patency lost; mucosa often damaged irreversibly.
Salpingitis isthmica nodosa (SIN):
- Diverticular outpouchings of tubal mucosa into the muscularis.
- Often a sequel to chlamydial infection.
- Clinical correlate: ectopic pregnancy risk increased significantly (impaired transport, abnormal implantation surfaces).
Genital tuberculosis
Distinct pathological pattern:
- Tubercles (granulomas with caseous necrosis) in tubes, endometrium, peritoneum.
- Tubes often grossly distorted — beaded, rigid, with caseous material in lumen.
- "Tobacco-pouch" appearance of fimbriae.
- Often bilateral.
- Clinical correlate: chronic pelvic pain, infertility, menstrual irregularity, sterile pyuria, raised inflammatory markers, weight loss, sometimes asymptomatic until presenting with infertility. Histology shows granulomas; culture for AFB; PCR (GeneXpert) increasingly used.
Mechanisms of long-term sequelae
Tubal factor infertility:
- Loss of ciliated epithelium → impaired oocyte pickup and transport.
- Luminal narrowing or occlusion.
- Distorted tubal architecture.
- Risk per episode: 10–15% after one episode of PID, rising to >50% after three.
- IVF often required.
Ectopic pregnancy:
- Impaired transport allows implantation in the tube.
- Risk increases 6–10× after PID.
- See ectopic-pathophysiology.
Chronic pelvic pain:
- Adhesions, hydrosalpinx, residual inflammation.
- Often coexists with central sensitisation. See chronic-pelvic-pain.
Hydrosalpinx:
- May be silent or cause chronic pain.
- Negatively impacts IVF success (toxic fluid leakage into uterine cavity).
- Salpingectomy or proximal occlusion before IVF improves implantation rates.
Fitz-Hugh-Curtis syndrome:
- Transperitoneal/lymphatic spread of organisms (classically chlamydia, but also gonorrhoea) to peri-hepatic peritoneum.
- "Violin-string" adhesions between liver capsule and abdominal wall.
- Clinical correlate: right upper quadrant pain mimicking cholecystitis, in a woman with pelvic infection (may be subtle pelvic findings).
Why bilateral?
Tubal infection is typically bilateral because:
- Organisms ascend through the cervix to both tubes simultaneously.
- Sigmoid restraint on the left and dextrorotation often produces asymmetric severity, but bilaterality is the rule.
- Unilateral involvement should raise suspicion of an alternative diagnosis (e.g., diverticulitis, appendicitis, or PID in a woman with prior salpingectomy on the other side).
Assessment
Correlating pathology to clinical features
- Cervical motion tenderness: broad ligament inflammation.
- Adnexal tenderness: tubal and adnexal inflammation.
- Cervical mucopus: cervicitis from ascending organisms.
- Hot, painful, palpable adnexal mass: pyosalpinx or TOA.
- Right upper quadrant pain: Fitz-Hugh-Curtis.
- Deep dyspareunia: posterior pelvic inflammation.
- Postcoital bleeding: chlamydial cervicitis (friable cervix).
- Tachycardia, fever, marked tenderness, free fluid: ruptured TOA — surgical emergency.
Investigations
- See acute-pelvic-infection.
- Imaging: TVS shows tubal thickening, "cogwheel" sign, free fluid, complex adnexal mass.
- Laparoscopy is the historical gold standard for PID diagnosis; rarely performed for diagnosis alone today but indicated when alternative diagnosis cannot be excluded, when surgical intervention may be needed, or for fertility workup.
Histology
Endometrial biopsy showing plasma cell endometritis is supportive of PID even when tubal histology not available. Performed in research settings; uncommon in routine practice.
Management
Management is detailed in acute-pelvic-infection. The pathological understanding informs:
- Early treatment matters — irreversible damage occurs even before clinical severity is high.
- Adequate duration (14 days minimum).
- Anaerobe cover essential for severe disease or TOA.
- Drainage of large abscesses.
- Surgical exploration for ruptured TOA.
- Investigation for TB in chronic or atypical disease.
- Counselling about long-term sequelae (infertility, ectopic, chronic pain) from the first episode.
Red flags / pitfalls
- Missing chlamydia as silent cause → late presentation with infertility or ectopic.
- Inadequate duration of antibiotics → chronic salpingitis sequelae.
- Missing TB-PID — granuloma on histology is diagnostic.
- Failure to treat partner → reinfection.
- Anchoring on PID with unilateral disease — consider alternative diagnoses.
- Forgetting Fitz-Hugh-Curtis — RUQ pain in young women with pelvic findings.
- Not counselling about long-term sequelae at first episode — patients should understand the stakes.
- Performing chromopertubation (HSG/HSI) during acute infection — disseminates organisms.
Evidence anchors
- RCOG Green-top Guideline No. 32 — Management of Acute Pelvic Inflammatory Disease.
- BASHH 2018 UK National Guideline for PID Management.
- CDC STI Treatment Guidelines (2021) — PID section.
- Westrom L, Eschenbach D. Pelvic Inflammatory Disease. In: Holmes, Sparling, et al. Sexually Transmitted Diseases. 4th ed.
- Wiesenfeld HC. Acute Pelvic Inflammatory Disease. N Engl J Med 2015 (clinical review).
- Mabey D, et al. Tubal pathology and outcomes after PID. Sex Transm Infect series.
- South African National Department of Health STI Guidelines (latest).
- WHO Guidelines on STI management.