Fibroid

Summary

Uterine leiomyomas (fibroids) are common benign, hormone-sensitive myometrial tumors affecting about 20% of women over 35, more prevalent in Black women. Risk factors include nulliparity, early menarche, obesity, hypertension, and family history. Often asymptomatic, they may cause heavy bleeding, pelvic pain, pressure symptoms, infertility, and anemia. Diagnosis is mainly by pelvic ultrasound. Management ranges from observation to medical therapy, minimally invasive procedures, or surgery, depending on symptoms, size, and fertility goals. Complications include anemia, infertility, degeneration, and rare malignant transformation; in pregnancy, they may cause miscarriage, preterm labor, or red degeneration.

Definition

Uterine leiomyomas are benign, monoclonal neoplasms of smooth muscle origin that often contain variable amounts of fibrous connective tissue. They are the most common tumor of the female genital tract and the leading indication for hysterectomy worldwide.

Fibroids are estrogen- and progesterone-dependent, growing during the reproductive years and typically regressing after menopause. They may be single or multiple and vary greatly in size—from microscopic nodules to large masses distorting the uterine contour.

Epidemiology

• Prevalence: 20% of women over the age of 35.

• Peak incidence: 30–50 years

• Ethnicity: Significantly higher prevalence, earlier onset, and greater severity in Black women

• Regression: Common after menopause due to hormonal decline

Risk Factors

Pathophysiology

Fibroids arise from a single myometrial smooth muscle cell undergoing monoclonal proliferation. Their growth is influenced by:

• Upregulated estrogen and progesterone receptors

• Increased extracellular matrix (ECM) deposition, giving a firm, fibrotic consistency

• Enhanced angiogenic activity and local growth factors (e.g., transforming growth factor-β, IGF, EGF)

• Progesterone promotes mitotic activity and ECM synthesis, while estrogen increases progesterone receptor expression.

Classification (by location)

1. Intramural (most common): Within the myometrium

2. Submucosal: Beneath the endometrium, often protruding into the uterine cavity → strongly associated with abnormal uterine bleeding and infertility

3. Subserosal: Beneath the serosal surface, protruding outward → causes pressure symptoms

4. Cervical: Located within the cervix

5. Pedunculated:  Attached by a stalk (intracavitary or subserosal); may become parasitic if supplied by adjacent organs

Clinical Features

Fibroids are asymptomatic in approximately 50% of cases. 

Symptoms, when present, depend on number, size, and location:

• Menstrual disturbances: Heavy menstrual bleeding (HMB), metrorrhagia, post-coital spotting, dysmenorrhea

• Pressure effects: 

• Bladder compression → frequency, urgency, retention

• Rectal pressure → constipation

• Ureteral compression → hydronephrosis (rare)

• Reproductive issues: 

• Infertility (≈30%, especially with submucosal fibroids)

• Recurrent miscarriage

• Preterm labor, malpresentation

• Pain: Pelvic pain, dyspareunia, acute pain from degeneration or torsion

• Other: Iron-deficiency anemia secondary to chronic blood loss

Diagnosis

Initial evaluation:

• Clinical Evaluation:

•  Bimanual examination: enlarged, irregular, firm, non-tender uterus

• Correlate with symptoms and menstrual history

• Pelvic ultrasound (transvaginal ± transabdominal): first-line imaging; shows well-circumscribed, hypoechoic  heterogeneous masses with posterior shadowing; degeneration may appear as cystic or calcified areas.

Further assessment:

• Hysteroscopy: Best for identifying submucosal fibroids and distinguishing from endometrial polyps.

• MRI: Gold standard for complex cases, surgical mapping, and differentiation from adenomyosis.

• Saline Infusion Sonohysterography (SIS): Improves visualization of submucosal fibroids.

• Laboratory: 

• CBC: To evaluate anemia

• β-hCG: Exclude pregnancy

• Coagulation profile: If abnormal uterine bleeding etiology is unclear

• Endometrial biopsy: Indicated in perimenopausal/postmenopausal women to rule out malignancy.

Differential Diagnosis

• Adenomyosis

• Endometrial polyps

• Endometrial carcinoma

• Ovarian masses
  

Management

General Principles

Management depends on:

• Symptom severity

• Fibroid size and location

• Age and proximity to menopause

• Desire for fertility preservation

Expectant Management

• Suitable for asymptomatic or small fibroids in women nearing menopause.

• Regular follow-up with pelvic exams and ultrasound.

Medical Management

Aimed at symptom control and preoperative shrinkage rather than cure:

• Hormonal: 

• Combined OCPs, progestins.

• Levonorgestrel-releasing intrauterine device (IUD) – reduces menorrhagia

• Antifibrinolytics: Tranexamic acid for HMB (contraindicated in high VTE risk)

• GnRH Agonists (e.g., leuprolide): Temporarily induce hypoestrogenism → shrinkage up to 50–70%; used preoperatively or for bridging to menopause

• GnRH Antagonists (e.g., elagolix, relugolix): Oral agents with add-back therapy to mitigate menopausal symptoms

• Selective Progesterone Receptor Modulators (e.g., ulipristal acetate): Effective in reducing size and bleeding (not FDA-approved in the U.S. due to rare hepatic toxicity)

• Nonhormonal: NSAIDs for dysmenorrhea

Minimally Invasive Interventions

• Uterine artery embolization (UAE): Shrinks fibroids by blocking blood supply; preserves uterus but has uncertain fertility outcomes.

• Radiofrequency ablation:  Laparoscopic or transcervical destruction of fibroids using thermal energy.

• MRI-guided Focused Ultrasound (MRgFUS): Noninvasive thermal ablation of fibroid tissue.

Surgical Options

• Myomectomy: 

• Preserves fertility;  indicated for symptomatic women desiring future pregnancy. 

• Approaches: Hysteroscopic, laparoscopic, or open approach depending on fibroid location. 

• Recurrence ≈25% in 3–5 years.

• Hysterectomy: Definitive treatment for women who have completed childbearing or failed conservative measures. 

Complications

• Reproductive: Infertility, miscarriage, preterm delivery

• Hematologic: Severe anemia from chronic bleeding

• Structural: Fibroid torsion, degeneration (hyaline, cystic, red, or calcific)

• Malignant transformation: Rare (<1%), usually leiomyosarcoma arising de novo rather than from pre-existing fibroid

• Urinary tract obstruction with large tumors

• Degenerative changes: hyaline, cystic, calcific, fatty, red (hemorrhagic – typically in pregnancy)

Fibroids in Pregnancy

Uterine fibroids occur in about 2–12% of pregnancies. Elevated estrogen and progesterone during gestation may cause fibroid growth, leading to pain, degeneration, or obstetric complications.

Antenatal period:

• First trimester: Hormonal stimulation promotes fibroid enlargement. Increased risk of miscarriage, pain from red degeneration or torsion of pedunculated fibroids.

• Second and third trimesters: Possible rapid growth, preterm contractions, placental abruption, malpresentation, or fetal growth restriction.

Peripartum:

• Fibroids may cause obstructed or dysfunctional labor, premature contractions, and a higher rate of cesarean delivery due to distortion of the uterine cavity or lower segment involvement.

Postpartum:

• Increased risk of uterine atony and postpartum hemorrhage, though most fibroids regress after delivery.

Management is usually conservative—analgesia, rest, and hydration—with surgical intervention reserved for severe complications.