Uterine leiomyoma (fibroids)

• A uterine leiomyoma is a benign tumour of smooth muscle in the wall of the uterus. Each fibroid arises from a single smooth muscle cell, so all fibroids are monoclonal.
• They are the most common pelvic tumour in women. By age 50, cumulative ultrasound evidence shows fibroids in approximately 70% of White women and 80% of Black women. ^[1]
• Fibroids respond to oestrogen and usually grow through the reproductive years, then shrink after the menopause. ^[1]
• Many cause no symptoms. About 15 to 30% of women with fibroids develop severe symptoms: heavy or prolonged bleeding, pelvic pressure or pain, urinary frequency, and infertility. ^[1]
• Symptoms and treatment depend on size, number and site, classified by FIGO Types 0 to 8. Submucosal fibroids (Types 0 to 3) most often cause heavy bleeding and infertility. ^[1][8]
• Treatment is individualised: watchful waiting for the asymptomatic; medical and non-hormonal drugs first for bleeding; procedural or surgical options (myomectomy, uterine artery embolisation, hysterectomy) when symptoms are severe or drugs fail. ^[1][2][3]

By the end of this page you should be able to:

1. Define uterine leiomyoma and explain its monoclonal origin, its dependence on oestrogen, and why it is rarely malignant.
2. Classify a fibroid by FIGO Type 0 to 8 and relate the site to the expected symptoms and treatment.
3. Recognise the typical clinical presentation and examination findings, and outline the red flags that demand urgent assessment.
4. Plan sensible investigations, including when pelvic ultrasound, saline infusion sonography, or magnetic resonance imaging is used and when endometrial sampling is required.
5. Manage heavy bleeding due to fibroids with drugs, dose and route, including non-hormonal, hormonal, GnRH agonist and antagonist, and antifibrinolytic therapy.
6. Compare uterine artery embolisation, myomectomy and hysterectomy, and explain how the choice is guided by fertility wishes, fibroid characteristics and safety.
7. Counsel about special situations: pregnancy, adolescents, women approaching the menopause, and women desiring fertility.

Uterine leiomyoma is more often called a uterine fibroid. It is a benign tumour of smooth muscle arising from the myometrium, the muscular wall of the uterus. Each one starts from a single mutated smooth muscle cell and grows into a firm, well-circumscribed whorled nodule, which is why fibroids are monoclonal. ^[1] They are the most common solid pelvic tumour in women: by the age of 50, cumulative incidence detected by ultrasound is roughly 70% in White women and 80% in Black women. ^[1]

Most fibroids are small or silent. Only about 15 to 30% of women who have fibroids develop severe symptoms. ^[1] The presentation is governed by the fibroid's size, number and position. A tumour that projects into or distorts the cavity (submucosal) tends to cause heavy menstrual bleeding and sometimes infertility. A tumour that lies predominantly in the wall or under the outer coat (intramural or subserosal) is more likely to cause pressure, urinary or bowel symptoms, or to be found incidentally. ^[1]

Because growth is driven by oestrogen and progesterone, fibroids enlarge through the reproductive years and usually shrink after menopause. ^[1] They are almost never malignant: sarcomatous change occurs in less than 1% of fibroids. ^[1] Despite that, they remain the leading indication for hysterectomy. ^[2]

The international reference point for both classification and treatment planning is the FIGO (International Federation of Gynecology and Obstetrics) system, which names the tumour's location relative to the endometrium and the serosa as Types 0 to 8. ^[1][8] Named treatment guidelines include ACOG (American College of Obstetricians and Gynecologists) Practice Bulletin No. 228 (2021, reaffirmed 2025) ^[2] and NICE guideline NG88 (2018, last updated July 2026). ^[3] They are used together with product information for the specific drugs.

A uterine fibroid is a benign monoclonal smooth muscle tumour of the uterus. It is not a cancer, it does not spread, and it is usually surrounded by a pseudocapsule. Fibroids may be subserosal, intramural, submucosal, intraligamentous, cervical or, rarely, in the fallopian tubes. Some are pedunculated, hanging on a stalk, and some are sessile. ^{[1] [3]}

The FIGO (PALM-COEIN) subclassification for the site of a fibroid is the standard way to describe it (Table 1). Types 0 to 3 are submucosal: they are in contact with the endometrium and/or protrude into the uterine cavity. Type 4 is entirely intramural. Types 5 to 7 are subserosal, in contact with the outer serosa. Type 8 includes tumours in other sites, such as the cervix or pedunculated parasitic fibroids. Hybrid fibroids (for example Type 2 to 5) are in contact with both the endometrium and the serosa. ^[1][8]

Hybrid types are written as two numbers separated by a hyphen; the first number refers to the relationship with the endometrium and the second to the relationship with the serosa. ^[8]

Clinical degeneration patterns matter more for a student's examination than for instant diagnosis: hyaline, myxomatous, calcific, cystic, fatty, red (usually only in pregnancy), and necrotic. Red degeneration in pregnancy presents with acute pain. ^[1]

Fibroids are common, and more common than most clinical impressions suggest. In the United States, the cumulative prevalence by age 50 is approximately 70% in White women and 80% in Black women when the diagnosis is made by ultrasound. ^[1] Worldwide estimates are lower and vary, because they depend on whether ultrasound or symptoms are used; a widely quoted symptomatic prevalence of severe symptoms is roughly 15 to 30% of women affected. ^[1]

• Age. Fibroids are rare before puberty. They appear in the late teens and twenties and accumulate through the reproductive years; incidence rises markedly after the age of 30 and falls after menopause, since growth depends on oestrogen. ^[1]
• Ancestry. Black women have higher incidence, an earlier age at diagnosis and larger tumours when they first present, and report more severe symptoms than White women. The reasons are probably a mix of genetic, hormonal and environmental factors, but no single explanation is settled. ^[1]
• Other risk factors. Early menarche, obesity and hypertension are associated with a higher risk of fibroids; high parity, three or more births, is associated with a lower risk. ^[1]
• Family. A first-degree relative with fibroids increases an individual's risk.
• Reproductive history. Nulliparity is also associated with higher risk compared with multiparity.
• Clinical impact. Fibroid-related problems are among the most common reasons for gynaecology outpatient attendance attributed to fibroids, and fibroids are the leading indication for hysterectomy. ^[1][2]

Because most women have multiple fibroids, prevalence counts each woman once but treatment counts each fibroid. ^[1]

No single external agent causes fibroids. The current working model is that a somatic mutation in a single smooth muscle cell of the myometrium turns that cell and its descendants into a fibroid. Oestrogen and progesterone receptors are present in fibroid tissue and growth is hormone dependent; both hormones stimulate proliferation and extracellular matrix deposition. ^[1]

• Modifiable or associated factors. Obesity raises risk, partly through aromatisation of androgens to oestrogen in adipose tissue. Hypertension is repeatedly associated.
• Protective. Multiparity and older age at first birth are protective.
• Medications. Tamoxifen, a selective oestrogen receptor modulator with agonist activity in the uterus, can stimulate fibroid growth; aromatase inhibitors shrink fibroids by blocking oestrogen synthesis.

Everything a fibroid does follows from three facts: it is a discrete mass within the myometrium, it responds to cyclic oestrogen and progesterone, and it can distort the cavity.

• Bleeding. Submucosal fibroids interfere with the normal haemostasis of the endometrium: they increase the surface area of bleeding, promote abnormal vessels in the overlying endometrium, and alter local forces that expel menstrual blood. Both volume and duration therefore increase. Heaviness that causes anaemia is common when a fibroid sits within or just below the endometrium. ^[1][3]
• Bulk and pressure. As a fibroid enlarges, the uterus enlarges with it. Anterior and fundal fibroids press on the bladder, causing urinary frequency and urgency; posterior fibroids press on the rectum, causing constipation and pelvic heaviness.
• Pain. Most fibroids are not painful. Pain arises from degeneration with haemorrhage into the tumour, from torsion of a pedunculated subserosal fibroid, or from uterine contractions against a large intramural mass during menstruation.
• Reproductive effects. Submucosal fibroids are associated with infertility, implantation failure and recurrent miscarriage by distorting the cavity. Intramural fibroids that do not reach the cavity have a smaller and less consistent effect.
• Pregnancy. Fibroids rarely change size in early pregnancy, but red degeneration, with acute pain and fever, is more common in pregnancy. Fibroids in the lower segment are associated with malpresentation, preterm labour, placental abruption and postpartum haemorrhage. ^[1]
• Menopause. Fibroids lose their hormonal supply; most shrink and symptoms resolve, which is why expectant management is sensible in a perimenopausal woman with mild symptoms. ^[1]

• Gross. A fibroid is a firm, pale grey-white, whorled, well-circumscribed nodule, usually within the myometrium, sometimes with a pseudocapsule.
• Microscopic. Interlacing bundles of smooth muscle cells with abundant collagenous extracellular matrix; mitoses are scarce in a benign tumour. Cellular variants and smooth muscle tumours of uncertain malignant potential are found only after surgery, which is why surgery on a presumed fibroid is undertaken with caution in postmenopausal women and in women with a rapidly enlarging mass. ^[1][2]
• Malignancy (sarcoma). Leiomyosarcoma is rare and cannot be reliably distinguished from a fibroid on imaging. The risk is low but rises with age; the estimated incidence of an unsuspected sarcoma in surgery performed for presumed fibroids ranges from 1 in 300 to fewer than 1 in 10,000 operations. ^[1] Evaluation must therefore be more careful in postmenopausal women and in those with rapid growth or atypical imaging, and morcellation is avoided where malignancy is suspected.

Women describe heavy menstrual bleeding as flooding, clots, and soaking through protection; changing pads or tampons at least hourly suggests heavy menstrual bleeding. ^[7] Bleeding that interferes with daily life, work, sport or sexual activity, and the associated tiredness of iron deficiency, matters more than counting millilitres. Fibroid-related bleeding is usually heavy and prolonged; intermenstrual or postcoital bleeding is less typical and should raise the question of polyp or malignancy as well.

Symptom clusters:

• Bleeding: heavy menstrual bleeding, sometimes prolonged; intermenstrual bleeding if the fibroid is submucosal and ulcerated; anaemia.
• Bulk and pressure: pelvic heaviness, an enlarging abdomen, a sensation of a lump; urinary frequency and urgency; constipation; dyspareunia; backache.
• Pain: dysmenorrhoea, acute pain from red degeneration or torsion; chronic pelvic pain when fibroids are multiple or large.
• Reproduction: infertility, recurrent miscarriage, and symptoms of pregnancy complications.
• Menopausal: many symptoms improve as ovarian activity falls; a new bleed after menopause is never attributed to fibroids without excluding cancer.

On pelvic examination, a fibroid uterus is enlarged, firm and irregular, but usually mobile. The mass most often arises from the anterior or posterior wall and feels solid. A fixed uterus, pronounced tenderness, an adnexal mass or rapid change in size are reasons to image rather than to conclude "fibroids". ^[1]

Look also for anaemia (pallor, tachycardia), thyroid or androgen excess if cycles are irregular, and for cervical or adnexal pathology. A pregnancy test is mandatory in any woman of reproductive age with abnormal bleeding.

The main task is to separate a benign fibroid from the other causes of heavy bleeding, pelvic mass and pain.

• Pregnancy test (urine, then serum quantitative human chorionic gonadotrophin if needed) in every woman of reproductive age with abnormal bleeding. ^[3]
• Full blood count and ferritin for anyone with heavy menstrual bleeding, because anaemia is common and is often found only on the laboratory test. ^[3]
• Coagulation screen when bleeding has been heavy since menarche or there is a personal or family history suggesting a bleeding disorder. ^[3]
• Hormone tests only when indicated, for example thyroid stimulating hormone or prolactin when cycles are irregular or galactorrhoea is present. Routine hormone testing is not recommended in isolated heavy menstrual bleeding. ^[3]
• Cervical screening and sexually transmitted infection tests when due or when infection is suspected.

• Transvaginal ultrasound is the preferred first-line imaging test. It identifies the presence, number, dimensions, vascularity and position of fibroids, and distinguishes them from adenomyosis with good reliability. ^[1][3]
• Saline infusion sonography (sonohysterography) improves visualisation of the uterine cavity and is useful when a submucosal fibroid is suspected, for example in abnormal uterine bleeding or infertility. It is a second-line tool, not first-line, for general investigation. ^[1][3]
• Hysteroscopy allows direct visualisation of submucosal fibroids and can become a see-and-treat procedure in the same session. ^[3]
• Magnetic resonance imaging is usually reserved for planning: before myomectomy or uterine artery embolisation when fibroid position, size and number are uncertain, and when there is concern about a variant or a malignant mass (atypical features, rapid growth, postmenopausal presentation). ^[1][3]
• Postmenopausal bleeding, with or without known fibroids, must be evaluated for uterine cancer regardless of imaging. ^[1]

Heavy bleeding is not always caused by the cavity being distorted. NICE recommends that endometrial sampling be undertaken in the context of diagnostic hysteroscopy, not as a blind biopsy, and only for women at risk of endometrial pathology: women aged 45 years or older with abnormal bleeding; and younger women with persistent intermenstrual or irregular bleeding, infrequent heavy bleeding with obesity or polycystic ovary syndrome, tamoxifen therapy, or treatment that has been unsuccessful. ^[3] AAFP guidance instead uses broader risk criteria, such as significant unopposed oestrogen exposure, persistent bleeding, or failed medical management, and recommends endometrial biopsy in all patients 45 years or older. ^[7] A woman with heavy but regular periods in her twenties, in whom the history suggests fibroids, can begin medical treatment without first investigating. ^[3]

Fibroids have no diagnostic cut-off in the laboratory sense, although imaging is diagnostic and the FIGO classification in Table 1 is the language used to communicate site and to plan treatment. ^[1][8] Nothing else in the staging scheme is needed for routine care.

• Histopathology is the only definitive confirmation: a smooth muscle tumour with no significant atypia and a low mitotic index. ^[2]
• Sarcoma suspicion must be raised in women over 50, in postmenopausal women, or when imaging shows rapid growth, a heterogenous mass, or a fixed pelvic mass. ^[1][2]

Management is decided by symptoms, fibroid size, number and location, desire for fertility, age, coexisting conditions and the woman's preferences. ^[2][3] The steps below follow the current guidelines.

• Asymptomatic fibroids require no treatment. Small and stable fibroids can be reviewed, typically every 12 months, and especially in the perimenopausal woman, because symptoms usually remit as fibroids shrink after the menopause. ^[1]
• For symptomatic fibroids, pharmacological treatment is usually tried before procedural or surgical treatment. ^[1]
• Definitive and lasting relief comes from procedures or surgery, chosen according to the symptoms.

All the drugs below reduce bleeding or suppress fibroid activity. They do not reliably shrink fibroids, except GnRH analogues.

• Tranexamic acid (an antifibrinolytic) can reduce uterine bleeding by up to 40%. ^[1] Oral tranexamic acid at 1 to 1.5 g three times daily during menstruation has reduced measured blood loss by 26% to 54% in studies of chronic heavy menstrual bleeding. ^[7] Long-term oral dosing used for heavy menstrual bleeding is 1 to 1.5 g three times daily during menstruation; acute, hospital-based dosing is 10 mg per kilogram intravenously every 8 hours or 20 to 25 mg per kilogram by mouth every 8 hours. ^[7]
• NSAIDs, for example naproxen 500 mg twice daily, ease dysmenorrhoea and may slightly reduce bleeding. ^[1][7]
• Both may be used as soon as they are found helpful, and NICE recommends continuing them while they help. ^[3]

• Combined hormonal contraception (oestrogen plus progestogen) regulates bleeding and appears to reduce overall blood loss.
• Progestogens can be given cyclically (10 to 14 days of each cycle) or continuously. Examples are medroxyprogesterone acetate 5 to 10 mg and megestrol acetate 40 mg by mouth; depot medroxyprogesterone acetate 150 mg intramuscularly every 3 months after a trial of oral therapy (to test tolerability). ^[1]
• Levonorgestrel-releasing intrauterine system (52 mg, releasing 20 micrograms per day). NICE recommends it as the first treatment for heavy menstrual bleeding with fibroids less than 3 cm in diameter that do not distort the cavity. ^[3] It is the most effective medical treatment for these smaller fibroids and reduces menstrual volume by about 70 to 95% (approximately 71 to 95% in trials of the 20 microgram per day device). ^[3][7]
• Progestogen-only methods that suppress menstruation can be considered for their amenorrhoeic effect.
• Levonorgestrel IUS is less suitable once fibroids are 3 cm or more, or if they distort the cavity, because the device may not sit correctly or work as well. ^[3]

• GnRH agonists (leuprolide 3.75 mg intramuscularly every month, goserelin 3.6 mg subcutaneously every 28 days) produce an early surge of oestradiol, then amenorrhoea after 7 to 14 days. ^[1][3] Used for 3 to 6 months, they shrink fibroids and improve anaemia. Because prolonged use causes hypo-oestrogenic bone loss, add-back therapy (low-dose oestrogen plus progestogen) is given when treatment continues. Rebound to pretreatment size within 6 months of stopping is common. ^[1][3]
• GnRH antagonists (oral) suppress oestrogen without the initial flare. Current licensed and NICE-recommended options:
  • ORIAHNN (elagolix 300 mg plus estradiol 1 mg plus norethisterone acetate 0.5 mg in the morning, and elagolix 300 mg in the evening) for up to 24 months for heavy menstrual bleeding with fibroids in premenopausal women. The bone loss is why the duration is limited to 24 months and why baseline and periodic bone mineral density testing are recommended. ^[4]
  • Relugolix-estradiol-norethisterone acetate, taken once daily, recommended by NICE as an option for moderate to severe symptoms, with no restriction on treatment duration. ^[5]
  • Linzagolix, 200 mg once daily with add-back for 6 months and then 100 mg once daily without; or 200 mg once daily with hormonal add-back throughout, for longer-term treatment. ^[6]
• Antiprogestins (mifepristone 5 to 50 mg once daily for 3 to 6 months) are used in some centres. ^[1]
• Selective oestrogen receptor modulators, danazol and aromatase inhibitors are further options with mixed evidence; danazol in particular has a high burden of androgenic adverse effects. ^[1]

• Before starting a combination therapy of this class, pregnancy must be excluded. Non-hormonal contraception is advised during treatment and for 28 days after it. ^[4]
• Bone mineral density is assessed at baseline and periodically when a GnRH antagonist is used beyond a few months. ^[4]
• GnRH antagonists are contraindicated in pregnancy, known osteoporosis, hormonally sensitive malignancy, uncontrolled hypertension, known liver disease, and several other situations listed in the product information. ^[4]

Uterine artery embolisation (UAE) is an image-guided, minimally invasive procedure in which embolic particles are delivered to the uterine arteries to cause fibroid infarction while normal myometrium is spared.

• When to offer. NICE and ACOG accept it as a treatment option for fibroids, after considering size, number, location and severity of symptoms; it is particularly considered for women who do not want surgery and who have no wish for further pregnancy. Women should be counselled that complication and re-intervention rates are higher than with hysterectomy in some comparisons, and that further procedures are sometimes needed. ^[2][3]
• Effectiveness. UAE reliably relieves heavy bleeding and bulk symptoms in most women who undergo it. Treatment failure or recurrence requiring further intervention occurs in up to 25%, and is more likely if the arteries are not embolised bilaterally. ^[1]
• Fertility. UAE is not the first choice when future pregnancy is desired. It has been associated with a higher rate of pregnancy loss and other adverse pregnancy outcomes in reviews of women treated with UAE who later conceive. ^[1] Women who want to become pregnant should therefore be offered myomectomy as the default uterine-sparing procedure.
• Assessment before the procedure. Ultrasound imaging first; MRI when the position, size, number or vascularity of fibroids, or the plan itself, is uncertain. ^[3]
• Risks. Infection, transient or permanent amenorrhoea from ovarian or uterine ischaemia, post-embolisation syndrome, and nontarget embolisation.

Myomectomy is surgical removal of the fibroids with conservation of the uterus. It is the standard option when fertility or uterine preservation is wanted.

• Routes. Hysteroscopic (transcervical) for Type 0, 1 and 2 submucosal fibroids, often as see-and-treat; laparoscopic or open abdominal for intramural and subserosal fibroids. ^[3]
• Preoperative planning. MRI is commonly used before surgery to plan the approach and locate deep or multiple fibroids. ^[1] Where the uterus is enlarged or distorted, a GnRH agonist is used preoperatively to shrink fibroids and correct anaemia. ^[3]
• Indications in practice. Recurrent heavy bleeding uncontrolled by drugs, pressure symptoms, a large mass with urinary or intestinal compression, infertility or recurrent miscarriage when a submucosal fibroid is likely to be the cause, and a patient's preference for conservation.
• Cautions. Multiple myomectomy is technically demanding and is associated with increased bleeding, adhesions and postoperative pain. New fibroids occur in a proportion of women, and about one quarter of women who have a myomectomy have a hysterectomy within 4 to 8 years. ^[1]
• Obstetric consequence. A scarred uterus carries a risk of uterine rupture in labour. Delivery and mode of birth should be discussed in advance, and the scar site communicated to the obstetric team.
• Morcellation. Fibroid tissue must be removed through small incisions. Morcellation must not be used if malignancy is suspected or if the patient has significant risk factors for uterine sarcoma; any patient prepared for fibroid surgery should have a preoperative assessment for uterine cancer. ^[2]

Hysterectomy is the definitive and most effective treatment. No new fibroid can grow afterwards. ^[1][2]

• When it is favoured. The woman does not desire further childbearing; there are other abnormalities such as endometriosis, cervical intraepithelial neoplasia, endometrial hyperplasia, or known genetic risk (BRCA mutation, Lynch syndrome); myomectomy would be complex because of extensive adhesions; or the woman chooses definitive treatment after discussion. ^[1]
• Route. Vaginal where feasible, otherwise laparoscopic or laparotomy, after an individual assessment and shared decision making. Total or subtotal hysterectomy (with or without the cervix) are discussed, and the ovaries are removed only with the woman's express wish and consent, with the risks explained. ^[3]
• Counselling points. Hysterectomy carries the risks of major surgery and has a higher serious complication rate when fibroids are present, including intraoperative haemorrhage and damage to adjacent organs; postoperative adhesion; loss of ovarian function even when the ovaries are retained; and psychological consequences. These are discussed fully before the decision. ^[3]
• Fertility. Hysterectomy ends fertility. This, combined with the woman's wishes about the uterus, is the central counselling discussion.

• Drug treatment is reviewed according to response; drugs that do not help at 3 to 6 months are stopped or changed. ^[1][3]
• GnRH analogues are not used beyond the licensed duration without add-back and monitoring.
• After surgery, routine review of bleeding, pain, and (in women planning pregnancy) reproductive plans.
• Pregnancy after myomectomy or UAE should be managed with awareness of the scar and of the association of fibroids with complications.

• Heavy menstrual bleeding and anaemia. The most common complication and the main reason fibroids are treated. ^[1]
• Bulk and pressure effects. Urinary frequency, urgency and retention; constipation; pelvic discomfort; an enlarging abdomen; hydronephrosis.
• Pain. Dysmenorrhoea, acute pain from degeneration or torsion, chronic pelvic pain.
• Reproductive. Infertility, recurrent miscarriage, abnormal implantation; in pregnancy, malpresentation, preterm labour, placental abruption and postpartum haemorrhage (especially with lower-segment fibroids). ^[1]
• Malignancy. Sarcomatous change is rare (less than 1%). ^[1] Rapid growth after menopause or atypical imaging does not prove cancer but requires specialist evaluation.
• Treatment complications. Surgical risks increase as the uterus enlarges; infection and post-embolisation syndrome after UAE; bone loss with long-course GnRH analogues; relapse or need for re-intervention after UAE or myomectomy.

The outlook is excellent. Most fibroids are benign, grow slowly, and become manageable. Faster growth after menopause is unusual and should prompt review. After menopause the tumour shrinks and symptoms usually settle, which makes observation sensible in older women. ^[1]

• Recurrence of fibroids after myomectomy is expected over time, and about one quarter of women who have a myomectomy have a hysterectomy within 4 to 8 years. ^[1]
• After UAE, up to 25% of women require further treatment, including hysterectomy. ^[1]
• Medical treatment needs to continue: fibroids tend to return to pretreatment size within 6 months of stopping a GnRH agonist. ^[1]
• Loss to follow-up is a practical risk: women who are well after a procedure may not attend for the planned review, so a simple follow-up plan should be agreed before discharge.

There is no primary prevention, no population screening and no daily test. What matters is awareness of risk and prompt treatment of symptoms. Women with persistent or recurrent heavy bleeding, pelvic mass or pain who belong to higher-risk groups should be assessed clinically, and fibroids found incidentally in a woman without symptoms need no intervention. ^[1][2] Focused discussion after a procedure gives women the chance to ask about recurrence.

Fibroids are common in pregnancy and are usually harmless. ^[1]

• Outcome. Most pregnancies proceed normally; only a minority are affected by pain, preterm labour, malpresentation or placental problems. ^[1]
• Red degeneration presents with acute pain and low-grade fever in the second trimester; management is analgesia, rest and observation, with surgery reserved for diagnostic uncertainty.
• Lower-segment fibroids can obstruct labour and are associated with higher rates of caesarean birth, and with postpartum haemorrhage. ^[1]
• Management in pregnancy is conservative (analgesia for pain, monitoring for complications). Surgery during pregnancy is avoided except for life-threatening problems such as torsion or severe degeneration that cannot otherwise be managed.
• Postpartum, fibroids may involute; reassess at 6 weeks and 6 months.
• Medical therapy of fibroids is generally avoided in pregnancy. Drugs of the GnRH antagonist class (such as ORIAHNN) are also contraindicated in pregnancy, and any unintended pregnancy during their use is stopped and re-evaluated. ^[4]

Fibroids are rare before menarche and uncommon in teenagers. Heavy bleeding since menarche should raise the possibility of a coagulation disorder (heavy menstrual bleeding since the first period is a key screening clue). Pelvic ultrasound is used where the history or examination suggests a mass. ^[3]

Fibroids shrink after menopause. Observation is appropriate for mild symptoms. Bleeding after the menopause is not attributed to fibroids: it requires investigation for endometrial cancer, including endometrial sampling where indicated, regardless of imaging. ^[1][3]

Myomectomy is the standard uterine-sparing surgery when fibroids are causing bleeding, pain or reproductive difficulty. GnRH medical therapy is used to improve anaemia and shrink fibroids before surgery. UAE is generally avoided as the first choice when pregnancy is desired. ^[1][2][3]

Transvaginal ultrasound is the single most useful test and is often available in secondary care; where it is absent, a pelvic examination and a careful history identify an enlarged irregular uterus, and referral should follow. Tranexamic acid and NSAIDs are cheap and widely available, and treat bleeding effectively. Iron replacement treats anaemia. Where surgery is unavailable locally, refer early to the nearest surgical centre, and agree a clear follow-up plan.

• Uterine fibroid is a benign monoclonal smooth muscle tumour of the myometrium. It is never treated as cancer unless red flags appear.
• By age 50, fibroids are found on ultrasound in approximately 70% of White women and 80% of Black women. ^[1]
• Most are asymptomatic; 15 to 30% of affected women develop severe symptoms, and submucosal (FIGO Types 0 to 3) fibroids cause the most bleeding and infertility. ^[1]
• FIGO Types 0 to 8 describe position (submucosal, intramural, subserosal, other, and hybrid). ^[1][8]
• Fibroids depend on oestrogen: they grow during the reproductive years and shrink after menopause; expectant management suits mild perimenopausal disease. ^[1]
• Transvaginal ultrasound is the first-line imaging test; MRI is for planning myomectomy or uterine artery embolisation, or when malignancy is suspected. ^[1][3]
• First-line treatment for heavy bleeding with small fibroids is tranexamic acid, NSAIDs, combined hormonal contraception, progestogens, or a levonorgestrel-releasing IUS. ^[1][3]
• GnRH agonists and antagonists shrink fibroids and stop bleeding; GnRH antagonists are limited by bone loss (24 months for elagolix combinations) and need monitoring. ^[3][4]
• Ulipristal acetate 5 mg (up to 4 courses) is restricted to premenopausal women with fibroids 3 cm or more when surgery or embolisation is unsuitable or declined, with liver function tests before and during treatment. ^[3]
• Uterine artery embolisation has up to a 25% failure or recurrence rate, and is generally not the first choice when pregnancy is desired. ^[1]
• Myomectomy preserves the uterus and fertility but carries a recurrence risk; about a quarter of patients have a hysterectomy within 4 to 8 years. ^[1]
• Hysterectomy is definitive but ends fertility and carries higher serious complication rates in the presence of fibroids. ^[2][3]
• Bleeding after the menopause should never be attributed to fibroids without ruling out cancer. ^[1][3]
• NICE NG88 is the UK reference for heavy menstrual bleeding with fibroids; ACOG Practice Bulletin No. 228 covers the medical, procedural and surgical management in the United States. ^[2][3]

Fibroids link closely to abnormal uterine bleeding, endometrial cancer, polycystic ovary syndrome, contraception and intrauterine systems, infertility and recurrent miscarriage, uterine inversion and rupture, obstetric haemorrhage, iron deficiency anaemia, and pelvic mass. These pages are related subjects on MedGrasp and are listed as plain text until verified.