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Structural and non-structural causes of bleeding

Organise abnormal uterine bleeding into structural and non-structural mechanisms, use pattern and risk to select imaging or hysteroscopy, and recognise when more than one cause is contributing.

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Classification follows stabilisation

Haemodynamic compromise, pregnancy-related bleeding, severe anaemia, sepsis, torsion or uncontrolled loss requires acute management before a detailed PALM-COEIN classification is completed.

Action: Resuscitate, test for pregnancy, obtain urgent bloods and senior gynaecology input, then use examination and imaging to identify the bleeding source and definitive control.

Open the sections you need. The overview is shown first.
01Purpose and principlesWhat the assessment is for and the core concepts behind it.

Abnormal uterine bleeding describes bleeding that differs in regularity, frequency, duration or volume from the person’s usual pattern after pregnancy-related and extrauterine sources are considered. The PALM-COEIN framework prevents a narrow focus on fibroids. Structural PALM causes can be demonstrated by imaging, hysteroscopy or histology. Non-structural COEIN causes reflect systemic haemostasis, ovulation, local endometrial function, treatment effects or less common mechanisms. The categories can be recorded together rather than made mutually exclusive.

Polyps are focal endometrial overgrowths that may cause intermenstrual, postcoital or heavy bleeding; small lesions can be missed by routine ultrasound, so hysteroscopy is more discriminating when the symptom pattern suggests the cavity. Adenomyosis places endometrial glands and stroma within myometrium, often producing painful heavy periods and a bulky tender uterus. Leiomyomas are benign smooth-muscle tumours; submucosal and cavity-distorting fibroids are particularly associated with bleeding, whereas larger intramural or subserosal disease may add pressure symptoms.

Malignancy and hyperplasia matter even though benign causes are more common. Risk increases with postmenopausal status, prolonged anovulation, obesity, PCOS, tamoxifen, diabetes and previous hyperplasia, but disease can occur without these. Persistent intermenstrual bleeding, failed treatment or suspicious imaging leads to direct cavity evaluation and histology. A thin or apparently regular premenopausal endometrium on ultrasound cannot exclude cellular disease because normal thickness varies across the cycle.

Coagulopathy may be inherited, such as von Willebrand disease or platelet dysfunction, or acquired through liver disease, thrombocytopenia and anticoagulants. Ask whether heavy bleeding began at menarche, and about epistaxis, bruising, dental and surgical bleeding, postpartum haemorrhage and family history. PT and APTT are incomplete screening tests for several disorders. Haematology can time von Willebrand testing and interpret results affected by stress, hormones and blood group.

Ovulatory dysfunction often produces irregular, infrequent and sometimes prolonged heavy bleeding because progesterone-organised shedding is absent. Adolescence and perimenopause can be physiological contexts, while PCOS, thyroid dysfunction, hyperprolactinaemia, major weight change, intense exercise, chronic illness and medicines are possible drivers. Testing is hypothesis-led. Chronic anovulation also changes endometrial protection needs, so symptom control without considering hyperplasia risk can be incomplete.

Endometrial dysfunction is a diagnosis of mechanism after pregnancy, structural disease, coagulopathy and ovulatory disturbance have been considered. The cycle is often regular, but local vasoconstriction, fibrinolysis, inflammation and tissue repair produce excessive loss. It explains why tranexamic acid and NSAIDs can help patients with normal imaging. There is no single routine blood test that confirms primary endometrial dysfunction.

Iatrogenic causes need a timeline. Copper intrauterine contraception can increase menstrual loss, while progestogen-only and combined hormonal methods often cause unscheduled bleeding during adjustment or with inconsistent use. Anticoagulants reveal or worsen uterine bleeding but do not protect against coexisting fibroid or cancer. Tamoxifen can cause endometrial polyps and pathology. Review dose, adherence, interactions, pregnancy risk and whether bleeding predates treatment before attributing causation.

The ‘not otherwise classified’ group includes uncommon entities such as arteriovenous malformation, caesarean-scar niche and some myometrial abnormalities. Consider them when bleeding is severe, recurrent and discordant with routine tests, particularly after uterine surgery or pregnancy. Doppler or specialist imaging and hysteroscopy may be needed. Uterine instrumentation in a possible arteriovenous malformation can worsen bleeding, making senior imaging review important.

Map mechanism to test. A focal cavity question leads to hysteroscopy; uterine enlargement, mass or adenomyosis leads to pelvic and usually transvaginal ultrasound; coagulopathy history leads to focused blood assessment; irregular cycles lead to endocrine or ovulatory evaluation; and postmenopausal bleeding leads to urgent cancer exclusion. Continue to ask whether the proposed cause fully explains severity and pattern.

Key points

  • PALM describes structural causes: polyp, adenomyosis, leiomyoma, and malignancy or hyperplasia; COEIN describes coagulopathy, ovulatory dysfunction, endometrial dysfunction, iatrogenic causes and causes not otherwise classified.
  • The framework organises mechanisms rather than declaring one final diagnosis; fibroids and anticoagulation, adenomyosis and anovulation, or a polyp and hormonal contraception can coexist.
  • Pregnancy-related, cervical, vaginal, vulval, urinary and rectal bleeding sit outside non-pregnant uterine classification and must be localised first.
  • Polyps often cause intermenstrual or postcoital bleeding, submucosal fibroids distort the cavity, and adenomyosis commonly combines heavy bleeding with substantial dysmenorrhoea.
  • Ovulatory dysfunction produces irregular timing and prolonged unopposed endometrial proliferation; causes include adolescence, perimenopause, PCOS, thyroid disease, hyperprolactinaemia, weight change and systemic illness.
  • Primary endometrial dysfunction is considered when ovulation appears regular and no structural or systemic explanation is found; it reflects local haemostatic and inflammatory mechanisms.
  • Iatrogenic bleeding includes hormonal-method adjustment, copper intrauterine contraception, anticoagulants, tamoxifen and medicines affecting ovulation or endometrium; temporal association does not exclude disease.
  • Use hysteroscopy when a focal cavity or endometrial lesion is suspected and ultrasound when myometrial enlargement, adenomyosis or pelvic mass is the leading question.
  • Endometrial histology, not thickness alone, diagnoses hyperplasia or malignancy; select biopsy based on bleeding pattern and risk and obtain it within an appropriate cavity pathway.
  • Treat the contributor that matches the patient’s goal while maintaining surveillance for unresolved or changing bleeding rather than forcing every case into a single category.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Polyp phenotype

Intermenstrual or postcoital spotting with otherwise regular cycles can reflect an endometrial or cervical polyp and favours direct visualisation.

Leiomyoma phenotype

Heavy periods with pelvic pressure, urinary frequency, an enlarged irregular uterus or cavity distortion suggests fibroids, with symptoms depending on location.

Adenomyosis phenotype

Progressive dysmenorrhoea, heavy bleeding and a diffusely bulky tender uterus supports adenomyosis rather than a discrete fibroid mass.

Anovulatory pattern

Widely variable cycle intervals followed by prolonged heavy episodes suggests inconsistent ovulation and requires endometrial-risk and endocrine context.

Coagulopathy pattern

Bleeding from menarche plus bruising, epistaxis, procedural haemorrhage or family history supports systemic haemostatic assessment.

Iatrogenic timing

Bleeding begins after a contraceptive, tamoxifen or anticoagulant change, but pregnancy, infection and structural pathology remain competing explanations.

Red flags requiring action

  • Postmenopausal bleeding, persistent intermenstrual bleeding, suspicious cervix, new pelvic mass or unexplained weight loss requires prompt cancer-pathway assessment.
  • Abnormal bleeding with pregnancy possibility may represent ectopic pregnancy, miscarriage, gestational trophoblastic disease or placental pathology and belongs in a pregnancy pathway.
  • Sudden pain, vomiting and an adnexal mass suggests torsion, while fever and pelvic tenderness raises infection or abscess; bleeding classification must not delay urgent care.
  • Heavy bleeding from menarche with mucosal bleeding or affected relatives raises an inherited bleeding disorder even when uterine imaging is normal.
  • Tamoxifen, prolonged anovulation, obesity, PCOS or previous endometrial hyperplasia increases endometrial risk and changes the threshold for hysteroscopy and sampling.
03Method and interpretationA systematic approach to the test and its findings.
Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

  1. 01
    Pregnancy testing and source localisationFirst step
    Why
    Remove pregnancy-related and non-uterine bleeding from the classification before uterine testing.
    Interpretation and limitations
    Positive hCG redirects care. Speculum, urinary or rectal assessment is selected from the history; apparent timing on a pad does not prove uterine origin.
  2. 02
    Outpatient hysteroscopy
    Why
    Identify and characterise endometrial polyps, submucosal fibroids and focal cavity lesions.
    Interpretation and limitations
    Direct vision is prioritised by NICE for cavity-pattern HMB. Biopsy can be targeted when endometrial risk is present; incomplete visualisation needs further action.
  3. 03
    Transvaginal pelvic ultrasound
    Why
    Map fibroids, assess myometrium for adenomyosis and evaluate ovaries and adnexa.
    Interpretation and limitations
    Report fibroid relationship to the cavity and adenomyosis features. A negative scan may miss a small polyp, superficial endometriosis or some uncommon vascular lesions.
  4. 04
    Full blood count and haemostatic tests
    Why
    Assess anaemia, thrombocytopenia and suspected inherited or acquired bleeding disorder.
    Interpretation and limitations
    Blood count is universal for HMB. Coagulation studies and von Willebrand testing are selected from history and may need specialist repeat interpretation.
  5. 05
    Endocrine and ovulatory assessment
    Why
    Investigate irregular cycles when symptoms suggest thyroid, prolactin, PCOS or other ovulatory dysfunction.
    Interpretation and limitations
    Choose tests from phenotype; NICE advises against routine female hormone and thyroid panels in all HMB. Chronic anovulation increases endometrial concern.
  6. 06
    Endometrial histology
    Why
    Diagnose hyperplasia, atypia or malignancy in a risk-bearing bleeding pattern.
    Interpretation and limitations
    Obtain adequate tissue through the applicable hysteroscopy or postmenopausal pathway. Benign or insufficient blind tissue may not exclude a focal lesion.
04Clinical next stepsHow the result changes management or prompts escalation.
01Classify patternSeparate source, timing and mechanismFirst stepBleeding is heavy, irregular, intermenstrual, postcoital or prolonged.
  1. 1Establish pregnancy status and anatomical source, then describe cycle regularity, duration, volume impact, pain and non-menstrual bleeding.
  2. 2Review pelvic symptoms, examination, bleeding history, endocrine phenotype and treatment exposure to populate plausible PALM and COEIN categories.
  3. 3Retain more than one contributor when evidence supports it and state which uncertainty each planned test will resolve.
02Structural routeImage or inspect the suspected compartmentSymptoms or examination suggest a polyp, adenomyosis, fibroid, hyperplasia or malignancy.
  1. 1Use outpatient hysteroscopy for focal cavity and endometrial risk, with biopsy considered under the relevant bleeding pathway.
  2. 2Use transvaginal ultrasound for myometrium, fibroid mapping and adenomyosis and broader pelvic ultrasound for a large or uncertain mass.
  3. 3Refer urgent cancer features and reconcile visual, imaging and histological results rather than allowing one discordant normal test to close review.
03Non-structural routeTest the history-led systemic or functional causeImaging is normal or bleeding features point to coagulation, ovulation, endometrium or treatment.
  1. 1Obtain full blood count and select haemostatic, thyroid, prolactin or androgen assessment only when the corresponding history is present.
  2. 2Review every contraceptive and medicine exposure, adherence, interaction and temporal relationship, while excluding pregnancy and infection where relevant.
  3. 3Treat the likely mechanism, protect endometrium in chronic anovulation and reopen structural evaluation if response or trajectory is inconsistent.
04Discordant routeLook for coexistence and uncommon diseaseBleeding severity or persistence is not explained by the initial finding or treatment response.
  1. 1Recheck whether the source and pregnancy status were established and whether cavity visualisation, myometrial imaging and histology were adequate.
  2. 2Consider combined PALM-COEIN contributors and less common vascular, scar-related or systemic disease with specialist radiology or hysteroscopy advice.
  3. 3EscalationEscalate treatment and referral according to anaemia, risk and patient priorities while maintaining named ownership of unresolved tests.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
  • Record the working PALM and COEIN contributors after each result, including why a category is supported, excluded or still unresolved.
  • Track bleeding pattern, pain, pressure, haemoglobin and quality-of-life response; failure of mechanism-matched treatment should reopen classification.
  • Review new medicines, contraceptive changes, anticoagulant intensity and endocrine symptoms whenever bleeding changes rather than preserving an old label.
  • Ensure hysteroscopy, imaging and histology reports describe the specific compartment and any technical limitation, with discordant results discussed.
  • Escalate new postmenopausal bleeding, persistent intermenstrual bleeding, mass, pregnancy symptoms or acute haemorrhage outside the routine classification review.
06Special situationsVariants, exceptions and circumstances that change the usual approach.

Categories can coexist

A fibroid may be incidental while anticoagulation drives severity, or anovulation may compound a polyp; treatment should reflect causal weight, not merely presence.

Location shapes fibroid effect

A smaller submucosal fibroid can cause more bleeding than a larger subserosal lesion because cavity distortion matters more than diameter alone.

Normal imaging has a category

Endometrial dysfunction produces genuine heavy bleeding without a visible lesion and can respond to antifibrinolytic or anti-inflammatory treatment.

Timing can reveal treatment effect

Bleeding after a method change may be iatrogenic, but persistence, pain or risk features still require independent disease assessment.

Rare vascular causes need caution

Profuse recurrent bleeding after pregnancy or uterine surgery can reflect an arteriovenous lesion, for which blind instrumentation may be hazardous.

07Common pitfallsFrequent interpretation and management errors.
  1. 01

    Treating PALM-COEIN categories as mutually exclusive and stopping after one incidental finding.

  2. 02

    Calling all irregular bleeding hormonal without checking pregnancy, cervix, infection and endometrial risk.

  3. 03

    Using routine PT and APTT alone to rule out von Willebrand disease or platelet dysfunction.

  4. 04

    Assuming anticoagulation explains bleeding so completely that structural or malignant causes need no assessment.

  5. 05

    Applying a premenopausal ultrasound thickness cut-off as a substitute for risk-based histology.

  6. 06

    Instrumenting the uterus during unexplained profuse post-pregnancy bleeding without considering vascular malformation.

Practice

Two practice questions

Question 1 of 20 correct
Obstetrics and gynaecologyOriginal SBA

PALM structural category

A patient has heavy regular periods, increasing dysmenorrhoea and a diffusely bulky tender uterus. Which PALM-COEIN category and investigation best fit the leading mechanism?

Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom