Abnormal bleeding and structural causes

Key Takeaways

  • PALM–COEIN distinguishes structural from non-structural bleeding causes.

  • Pregnancy testing is important in reproductive-age bleeding presentations.

  • Symptoms and fertility goals influence treatment of fibroids and adenomyosis.

Last updated: October 2026

Abnormal Uterine Bleeding, Pelvic Pain & Endometriosis

Abnormal uterine bleeding (AUB) and chronic pelvic pain represent frequent presentations in Australian general practice and gynaecological outpatient clinics. A structured clinical approach requires distinguishing structural uterine pathologies from systemic and endocrinological disorders, stratifying oncological risk, and delivering evidence-based medical and surgical therapies.


FIGO PALM-COEIN Classification of Abnormal Uterine Bleeding

The International Federation of Gynecology and Obstetrics (FIGO) PALM-COEIN system classifies abnormal uterine bleeding into nine distinct categories. The first four categories represent structural abnormalities that can be imaged or sampled histologically (PALM), whereas the remaining five represent non-structural systemic, endocrine, or functional disturbances (COEIN).

Structural Etiologies (PALM)

  1. Polyp (AUB-P): Endometrial or endocervical polyps are focal hyperplastic outgrowths of endometrial glands and stroma containing thick-walled vascular channels. While most are benign, atypical hyperplasia or malignancy occurs in approximately 1% to 3% of premenopausal and 4% to 5% of postmenopausal patients. Transvaginal ultrasound (TVUS) or saline infusion sonohysterography (SIS) demonstrates a well-defined intracavitary lesion with a solitary vascular feeding pedicle on colour Doppler. Management consists of hysteroscopic polypectomy with histological examination.
  • Adenomyosis: Ultrasound assesses myometrial features; MRI can evaluate the junctional zone. A thickness above about 12 mm is an MRI feature, not a stand-alone universal ultrasound definition.
  1. Leiomyoma (AUB-L): Benign monoclonal smooth muscle neoplasms of the myometrium (fibroids), subdivided by the FIGO subclassification based on anatomical position (Types 0 to 8):
    • Submucosal (Types 0, 1, 2): Lie directly beneath or distort the endometrium; even small submucosal lesions disrupt endometrial haemostasis and produce profound menorrhagia and subfertility.
    • FIGO locations: Types 3 and 4 are intramural; type 3 contacts the endometrium. Type 5 is subserosal with at least half its diameter intramural, type 6 has less than half intramural and type 7 is pedunculated subserosal.
    • Subserosal (Types 6, 7): Project outward from the peritoneal surface; typically cause compressive bulk symptoms (urinary frequency, constipation, hydronephrosis) rather than abnormal bleeding.
    • Medical management: Tranexamic acid, combined oral contraceptives (COCP), oral progestogens, or LNG-IUS for menorrhagia. Gonadotrophin-releasing hormone (GnRH) agonists (goserelin) or antagonists (relugolix) induce temporary hypoestrogenism, reducing fibroid volume by 30% to 50% prior to surgery or in perimenopausal transition.
    • Surgical management: Hysteroscopic resection for Type 0 and 1 submucosal fibroids; laparoscopic or open abdominal myomectomy for women desiring future fertility; uterine artery embolisation (UAE) or hysterectomy for definitive management in completed families.
  2. Malignancy & Hyperplasia (AUB-M): Encompasses endometrial hyperplasia (with or without cytological atypia) and endometrial carcinoma. Atypical endometrial hyperplasia carries a 30% to 45% risk of concurrent invasive adenocarcinoma on definitive hysterectomy specimen.

Non-Structural Etiologies (COEIN)

  1. Coagulopathy (AUB-C): Encompasses systemic disorders of haemostasis, notably von Willebrand disease (vWD), platelet function defects, and immune thrombocytopenia. Up to 20% of adolescents presenting with severe menorrhagia requiring hospital admission have an underlying coagulopathy. Clinical screening criteria include heavy bleeding since menarche, personal history of postpartum haemorrhage or surgical bleeding, frequent epistaxis, or bleeding gums.
  2. Ovulatory Dysfunction (AUB-O): Common at the extremes of reproductive life (adolescence and perimenopause) and in endocrinopathies such as polycystic ovary syndrome (PCOS), hypothyroidism, and hyperprolactinaemia. Anovulation results in persistent, unopposed oestrogen stimulation of the endometrium without corpus luteum formation or progesterone production. The endometrium outgrows its vascular supply, leading to erratic, unpredictable, and often profuse breakthrough bleeding.
  3. Endometrial Primary Dysfunction (AUB-E): Manifests as cyclic, predictable, heavy menstrual bleeding in women with normal ovulatory cycles and no identifiable structural lesion. The primary defect involves local endometrial haemostasis, including deficient production of vasoconstrictors (prostaglandin PGF2αPGF_{2\alpha} and endothelin-1), excessive production of vasodilators (prostaglandin PGE2PGE_2 and prostacyclin), or accelerated tissue plasminogen activator (tPA)-mediated fibrinolysis.
  4. Iatrogenic (AUB-I): Caused by therapeutic interventions, including copper intrauterine devices, breakthrough bleeding from progestogen-only implants or depot injections, systemic anticoagulants, selective serotonin reuptake inhibitors, or herbal supplements.
  5. Not Otherwise Classified (AUB-N): Rare conditions such as uterine arteriovenous malformations (AVMs), chronic endometritis, and cesarean scar defects (isthmocele) that do not fit into other categories.

Diagnostic Workup and Endometrial Biopsy Thresholds

The diagnostic algorithm for abnormal uterine bleeding begins with a targeted clinical history, physical examination, and mandatory exclusion of pregnancy in all women of reproductive age via urine or serum human chorionic gonadotrophin (β\beta-hCG).

Laboratory and Imaging Evaluation

  • Full Blood Count & Ferritin: Assesses the severity of iron deficiency anaemia secondary to chronic heavy blood loss.
  • Coagulation Studies: Indicated in adolescents with severe menorrhagia, patients with a personal or family history of bleeding disorders, or prior to invasive surgical procedures.
  • Endocrine Biomarkers: Thyroid-stimulating hormone (TSH), prolactin, and androgen profile (free testosterone, sex hormone-binding globulin) indicated when ovulatory dysfunction or PCOS is suspected.
  • Pelvic Transvaginal Ultrasound (TVUS): The initial imaging modality of choice to evaluate endometrial stripe thickness, endometrial texture, myometrial homogeneity, junctional zone integrity, and ovarian morphology. Saline infusion sonohysterography (SIS) or outpatient hysteroscopy is indicated if the endometrium is thickened, heterogeneous, or if intracavitary polyps or submucosal fibroids are suspected.

Primary references (checked 7 October 2026): 2023 international PCOS guideline.

Test Your Knowledge

A 43-year-old multiparous woman presents with an 18-month history of worsening menorrhagia and severe secondary dysmenorrhoea that is poorly responsive to oral non-steroidal anti-inflammatory drugs. She describes having to change pads every hour on days 2 and 3 of her cycle, passing large clots. Her past medical history is unremarkable, and she does not desire future fertility. Bimanual pelvic examination reveals a symmetrically enlarged, globular, boggy, and diffusely tender uterus approximately equivalent in size to a 12-week gestation. Transvaginal pelvic ultrasound reveals an asymmetric myometrial thickening, subendometrial echogenic linear striations, and an irregular, thickened junctional zone measuring 14 mm. There are no discrete focal fibroids or endometrial polyps. Which of the following is the most likely underlying diagnosis?

A

Adenomyosis characterized by ectopic myometrial endometrial invasion

B

Endometrial carcinoma causing malignant irregular tissue proliferation

C

Submucosal leiomyoma producing distorted intracavitary architecture

D

Pelvic inflammatory disease resulting in chronic bilateral salpingitis

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