FIGO classification of abnormal uterine bleeding (PALM-COEIN) (also searched with possessive/alternate eponym spelling where applicable, ICD-10: N93.9) is an internationally standardized, consensus-derived diagnostic and classification framework established by the International Federation of Gynecology and Obstetrics (FIGO) to categorize the underlying aetiologies of abnormal uterine bleeding (AUB) in non-pregnant, reproductive-aged women^2,3,4. AUB describes any structural, hormonal, or systemic variation from normal menstrual cycle parameters—encompassing volume, regularity, frequency, and duration—persisting for at least 6 months². By replacing antiquated, imprecise terminology such as menorrhagia and metrorrhagia, the PALM-COEIN system stratifies causes into two distinct categories: structural anomalies that can be imaged or histologically diagnosed (PALM: Polyp; Adenomyosis; Leiomyoma; Malignancy and hyperplasia) and non-structural entities evaluated via laboratory, clinical, and functional assessments (COEIN: Coagulopathy; Ovulatory dysfunction; Endometrial; Iatrogenic; Not yet classified)^4,5. This standardized architecture streamlines clinical evaluation, guides targeted medical and surgical management, and enhances global research comparability^2,3.

Etiology & Risk Factors

• Structural Causes (PALM):
  • Polyp (AUB-P): Benign hyperplastic overgrowths of endometrial glands and stroma lined by epithelium, often associated with focal intermenstrual bleeding or postmenopausal spotting. Risk factors include advancing age, obesity, and tamoxifen exposure.
  • Adenomyosis (AUB-A): Presence of ectopic endometrial glands and stroma deep within the myometrium, inducing smooth muscle hypertrophy. Associated with painful dysmenorrhea and heavy menstrual bleeding (HMB), particularly in multiparous women over 35 years of age⁶.
  • Leiomyoma (AUB-L): Monoclonal benign smooth muscle tumours of the myometrium (fibroids), further subclassified based on anatomical location into submucosal (subclass L_sm, most strongly associated with HMB due to cavity distortion), intramural, and subserosal variants. Common in African-American women, nulliparity, and obesity.
  • Malignancy and Hyperplasia (AUB-M): Premalignant atypical endometrial hyperplasia or endometrial carcinoma. Major risk factors include unopposed estrogen exposure (obesity, polycystic ovary syndrome, tamoxifen), Lynch syndrome, and advanced age.
• Non-Structural Causes (COEIN):
  • Coagulopathy (AUB-C): Systemic haemostatic disorders, most notably von Willebrand disease, platelet function defects, or anticoagulant therapy. Often manifests as heavy menstrual bleeding starting from menarche.
  • Ovulatory Dysfunction (AUB-O): Endocrine abnormalities disrupting hypothalamic-pituitary-ovarian (HPO) axis function, including polycystic ovary syndrome (PCOS), hyperprolactinaemia, thyroid disorders, hypothalamic amenorrhoea, and perimenopausal transition. Results in predictable or unpredictable anovulatory breakthrough bleeding.
  • Endometrial Disorders (AUB-E): Primary peripheral local endometrial abnormalities characterized by regular predictable ovulation but abnormal localized regulation of vasoconstriction and fibrinolysis (e.g., deficiency in local vasoconstrictors like endothelin-1 or excessive plasminogen activator activity).
  • Iatrogenic (AUB-I): Bleeding caused by exogenous pharmacological agents, including copper or levonorgestrel intrauterine devices (IUDs), systemic anticoagulants, antiplatelet drugs, antipsychotics causing hyperprolactinaemia, and hormonal contraceptives.
  • Not Yet Classified (AUB-N): Rare, poorly defined, or uncharacterized entities (such as arteriovenous malformations, myometrial hypertrophy, or chronic endometritis) that do not fit neatly into the other categories.

Pathophysiology

The pathophysiological pathways leading to abnormal uterine bleeding vary widely across the PALM-COEIN spectrum, reflecting distinct mechanical, hormonal, and molecular insults to the endometrium and myometrium^4,7. In structural disorders like submucosal leiomyomas (AUB-L_sm) and polyps (AUB-P), mechanical expansion of the uterine cavity increases surface area, stretches the overlying capillary network, and impairs local vascular compression during menses, precipitating prolonged heavy blood loss. Adenomyosis (AUB-A) disrupts normal subendometrial myometrial contraction waves, preventing effective occlusion of spiral arterioles and leading to dysmenorrhea and dysfunctional shedding. In non-structural ovulatory disorders (AUB-O), continuous, unopposed estrogen stimulation drives unchecked proliferation of the endometrium without subsequent progesterone-mediated stabilization, culminating in asynchronous, fragile tissue breakdown and irregular breakthrough bleeding. Endometrial dysfunction (AUB-E) arises from local molecular defects—specifically deficiencies in local vasoconstrictors (endothelin-1) and excessive matrix metalloproteinase or plasminogen activator activity—causing premature degradation of endometrial extracellular matrix and prolonged bleeding despite normal systemic coagulation and regular ovulation. Coagulopathies (AUB-C) compromise the primary haemostatic plug formation required to arrest normal physiological shedding from spiral arteries during menstruation, manifesting as severe, treatment-resistant heavy bleeding.

Clinical Presentation & Classic Clinical Signs

• History & Cardinal Symptoms:
  • Heavy menstrual bleeding (HMB): Blood loss exceeding 80 mL per cycle, soaking through pads/tampons every 1–2 hours, or passage of clots greater than 2.5 cm in diameter.
  • Intermenstrual bleeding (IMB): Bleeding occurring between clearly defined, predictable menstrual periods.
  • Chronic symptoms: Fatigue, exertional dyspnoea, pallor, and iron-deficiency anaemia secondary to persistent blood loss.
  • Pelvic pain, pressure symptoms, urinary frequency, or dyspareunia indicative of bulk lesions (leiomyomas, adenomyosis).
• Physical Examination & Named Clinical Signs:
  • General examination for signs of anaemia, conjunctival pallor, bruising (suggesting coagulopathy), thyroid enlargement, or features of hyperandrogenism (hirsutism, acne in PCOS).
  • Abdominal examination to palpate an enlarged, irregular, or firm uterus (fibroids or adenomyosis) extending above the pubic symphysis.
  • Speculum examination to inspect the vulva, vagina, cervix, and endocervical canal, explicitly ruling out cervical polyps, inflammation, trauma, or visible exophytic cervical/vaginal tumours.
  • Bimanual pelvic examination to assess uterine size, contour, mobility, and tenderness (characteristic boggy, globular, tender uterus in adenomyosis) and evaluate for adnexal masses.

Diagnostic Workup & Interpretation (Laboratory, Imaging & ECG/Pathology)

Staging, Classification & Clinical Scoring Systems

Differential Diagnosis

Management & Treatment Protocol

• Initial Stabilization & Resuscitation:
  • For acute, heavy, life-threatening bleeding episodes, assess hemodynamic stability. Administer intravenous conjugated equine estrogens (25 mg IV every 4–6 hours until bleeding stops) or high-dose combined oral contraceptives (e.g., ethinyl estradiol 30–35 mcg plus norgestimate/levonorgestrel TID for 7 days, then taper).
  • Provide aggressive fluid resuscitation with crystalloids and blood transfusion if haemoglobin drops below 7–8 g/dL or if signs of acute hypovolaemia are present.
  • Administer tranexamic acid (1.3 g IV or PO TID to QID) to stabilize clot formation.
• First-Line Medical / Pharmacological Therapy (with exact adult dosing):
  • Non-Hormonal Options: Tranexamic acid 1.3 g PO TID during heavy bleeding days (reduces menstrual blood loss by 40–50%); Nonsteroidal anti-inflammatory drugs (NSAIDs) such as mefenamic acid 500 mg PO TID or ibuprofen 600 mg PO TID starting on day 1 of menses to reduce prostaglandin-mediated bleeding and dysmenorrhea.
  • Hormonal Options: Combined oral contraceptives (COCs) containing ethinyl estradiol 20–30 mcg combined with a progestin, taken daily cyclically or continuously to regulate endometrial proliferation; Levonorgestrel-releasing intrauterine system (LNG-IUS, e.g., Mirena 52 mg) as highly effective first-line therapy reducing menstrual blood loss by over 80% and providing endometrial protection; Oral progestins such as norethindrone acetate 5–10 mg daily from cycle day 15 to 25 or medroxyprogesterone acetate 10 mg daily for 10–14 days per month, or depot medroxyprogesterone acetate 150 mg IM every 3 months.
• Surgical / Interventional Indications:
  • Hysteroscopic polypectomy for AUB-P; hysteroscopic myomectomy for Type 0, 1, or 2 submucosal fibroids.
  • Uterine artery embolization (UAE), magnetic resonance-guided focused ultrasound surgery (MRgFUS), laparoscopic myomectomy, or hysterectomy for symptomatic leiomyomas (AUB-L) unresponsive to medical therapy or causing severe bulk symptoms.
  • Endometrial ablation (thermal, radiofrequency) as a conservative surgical alternative for women with normal uterine cavities who have completed childbearing and failed medical management.
  • Total hysterectomy as definitive surgical management for refractory cases, adenomyosis, or premalignant/malignant pathology (AUB-M).

Complications & Prognosis

• Acute Complications: Severe iron-deficiency anaemia requiring parenteral iron infusion or blood transfusion, acute hypovolaemic shock from massive haemorrhage, and severe pain crises due to passing clots or degenerating leiomyomas^2,4.
• Chronic Complications: Persistent fatigue, reduced health-related quality of life, impaired occupational and social functioning, and chronic pelvic discomfort^2,4. Long-term unopposed estrogen exposure in untreated AUB-O or complex atypical endometrial hyperplasia carries a substantial risk of progression to endometrial adenocarcinoma (AUB-M)⁵.
• Prognosis: Excellent when underlying structural lesions are appropriately resected or non-structural endocrine/heamostatic disorders are systematically managed. Most patients achieve excellent cycle control and normalisation of haemoglobin levels with tailored medical therapy or minimally invasive surgical interventions^2,5.