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The principal modes are growth within the uterine wall, towards the cavity, and towards the outer surface: intramural uterine fibroids, submucosal uterine fibroids and subserosal uterine fibroids. “Fibrous tumour” is the historical label; the usual modern lesion is a leiomyoma, a benign growth of smooth muscle with a variable connective-tissue component, rather than a mass of collagen alone.^[ref]

An intramural uterine fibroid enlarges within the myometrium. It can remain enclosed by uterine muscle, push the cavity aside, or expand both inner and outer contours. Several nodules can give an irregularly enlarged uterus. Expansion compresses surrounding tissue into a cleavage plane or pseudocapsule; this differs from the destructive infiltrative growth typical of a malignant lesion.

A submucosal uterine fibroid grows towards the endometrium, projecting into and distorting the uterine cavity. It may remain broad-based or acquire a stalk as the surrounding wall is displaced. A pedunculated uterine fibroid can be pushed through the cervical canal and appear in the vagina as a uterine polyp. A polyp formed in this way is a mode of presentation of the same smooth-muscle tumour, not necessarily a different histological species. Its relation to the cavity helps explain why a comparatively small lesion may be associated with substantial bleeding.

A subserosal uterine fibroid projects outwards beneath the serosal covering. It may have a broad attachment or a long pedicle and become a large extrauterine-looking mass. Lateral outward growth can extend between the layers of the broad ligament; cervical growth can displace neighbouring pelvic structures. Rarely, a detached pedunculated lesion gains a blood supply from adjacent tissues and persists as a parasitic growth; this is not ordinary distant metastasis.^[ref]

The three directions are not mutually exclusive: a large nodule may affect both the uterine cavity and its external surface. Modern location classifications describe its relation to endometrium, myometrium and serosa more precisely, but those later type numbers are unnecessary to explain the anatomical modes requested here.

Growth is also distinct from secondary change. A poorly supplied area can undergo hyaline or cystic degeneration, haemorrhagic change or calcification; these changes alter consistency without establishing a new malignant mode of growth. Uterine fibroids often respond to the reproductive hormonal environment and commonly shrink after menopause, but neither every lesion's course nor its rate of growth is identical.^[ref] Location and attachment describe the mode of expansion; tissue examination establishes the nature of the tumour.

Classify the bleeding by anatomical source and by its relation to pregnancy, childbirth and menstruation; treatment must address that source. The amount of visible genital haemorrhage does not measure all the loss: a ruptured ectopic pregnancy or concealed placental abruption can cause major internal blood loss. Initial assessment of severe bleeding concerns the circulation, anaemia and the need for resuscitation while the cause is established. Bleeding from the urethra or rectum must first be distinguished from genital bleeding.

Local sources outside the uterine cavity. The vulva and vagina may bleed from lacerations after childbirth or other trauma, an inflamed lesion, a foreign body, a vascular lesion or cancer. Examination localizes the loss; treatment is local compression and repair of a significant laceration, removal of the foreign body, cause-directed treatment of infection, or specialist management of the lesion. A cervical polyp, cervical ectropion, cervicitis or cervical cancer can cause bleeding from the cervix, often noticed between periods or after intercourse. A suitable polyp can be removed and examined; inflammation requires its cause to be established, while a suspicious lesion requires diagnostic assessment rather than indiscriminate cauterization. After menopause, thin, fragile vulvovaginal tissues can also bleed; this does not remove the need to investigate a suspicious lesion. These are different conditions, not one disease called “uterine haemorrhage”. ^[ref]

Bleeding from the endometrium. Heavy or irregular menstruation may accompany ovulatory dysfunction, uterine fibroids, endometrial polyps, adenomyosis, a coagulopathy, medication effects or endometrial cancer. Modern assessment includes the menstrual and drug history, a full blood count, and selected ultrasound, hysteroscopy or tissue sampling according to the suspected cause. Where appropriate, menstrual bleeding can be reduced with tranexamic acid or hormonal treatment; an intracavitary polyp or uterine fibroid may instead need targeted removal. Persistent postmenopausal bleeding must not simply be treated as an ordinary period. ^[ref]

Early pregnancy. A miscarriage may bleed while pregnancy tissue separates or remains in the uterus. In a stable, confirmed case, expectant, medical or surgical management may be appropriate; heavy continuing loss or infection changes the urgency. Ectopic pregnancy requires a separate plan: selected stable cases may be monitored or treated medically, but rupture with haemorrhagic collapse requires urgent operative control, not treatment of the vagina as though it were the principal source. A hydatidiform mole is another pregnancy-related source of abnormal bleeding; current management includes removal by suction evacuation and subsequent human chorionic gonadotropin surveillance for persistent disease. ^{[ref] [ref] [ref]}

Later pregnancy and labour. Placenta praevia commonly produces relatively painless bleeding, whereas placental abruption more often causes pain and uterine tenderness; these are useful patterns, not infallible rules. Management depends on the mother's circulation, the fetus, the placental lesion and the stage of pregnancy, with urgent delivery when required. A blind digital cervical examination is inappropriate before a possible placenta praevia has been excluded. Ruptured vasa praevia causes fetal rather than maternal bleeding and demands a different interpretation. A small blood-stained mucous “show” during cervical change is not equivalent to these pathological losses. ^{[ref] [ref]}

After delivery. The principal categories are failure of uterine contraction, retained placental tissue, trauma and disordered coagulation. For uterine atony, the aim is to restore contraction with uterine massage and an appropriate uterotonic. Retained tissue, a genital laceration or uterine inversion requires correction of that particular cause; a coagulopathy requires haemostatic support. With placenta accreta spectrum, attempted forcible separation can provoke severe haemorrhage. Current care combines resuscitation with cause-directed measures, and can require tranexamic acid, balloon tamponade, embolisation or surgery when initial measures fail. Later postpartum bleeding also raises retained tissue and endometritis. ^[ref]

The 1865 distinction. An answer of the period could distinguish menstrual loss, local lesions, pregnancy-related haemorrhage and post-delivery failure of contraction through the history and physical examination. Compression, local plugging, removal of an accessible lesion and obstetric intervention were among the available approaches; their use was debated. The 1864 discussion of placenta praevia documents such disagreement. Modern imaging, blood banking, the present drug regimens and current operative pathways must not be attributed to that practice. Nor should historical astringents or depletion be substituted for identifying the source. ^[ref]

Absent menstruation is a sign with several causes; treatment must distinguish physiological absence, failure of menstrual cycling and obstruction of outflow. The word “suppression” does not establish that retained blood is poisoning the body or that producing a bleed will cure the underlying problem.

First distinguish primary amenorrhoea, where menstruation has never begun, from secondary amenorrhoea, where established cycles have stopped. Ask about the previous pattern, possibility of pregnancy, breastfeeding, age, illness, nutrition, exercise, medicines and associated symptoms. Pregnancy, lactation and menopause can explain physiological absence. Pregnancy must be considered before any proposed menstrual stimulant, with assessment for complications when pain or abnormal bleeding accompanies the missed period.^[ref]

A second group has impaired hormonal signalling or ovarian function. Severe illness, inadequate energy intake, major exertion and stress can suppress the hypothalamic–pituitary–ovarian axis. Other possibilities include thyroid disease, hyperprolactinaemia, primary ovarian insufficiency and chronic anovulation. These modern categories separate processes that an 1866 clinician might group under debility, constitutional disease or disordered ovarian activity. Anaemia and wasting deserve investigation and treatment when present, but are not universal explanations for every missed period.

A third group has an anatomical explanation. Cyclical pain with absent visible menstruation can indicate retained menstrual material behind an imperforate hymen or other outflow obstruction. Congenital absence or abnormal development of reproductive organs is different again. Acquired scarring of the uterine cavity may interrupt bleeding after instrumentation or disease. The response to obstruction is diagnosis-specific correction by an appropriate specialist; neither a “tonic” nor a drug intended to provoke uterine contraction repairs an absent or blocked passage.^[ref]

In period terms, treatment of a genuine associated illness, improved nourishment and protection from exhausting conditions could be sensible. Warm baths and drugs called emmenagogues were also employed, but their use should not be mistaken for proof of efficacy, or attempted before excluding pregnancy. Menstrual absence should not automatically be interpreted as the cause of mental or systemic illness.

Modern correction: investigate the relevant physiological pathway and treat its cause. Selected investigations include a pregnancy test, prolactin, thyroid-stimulating hormone, ovarian and pituitary hormone measurements and pelvic ultrasonography. For functional hypothalamic suppression, restore energy availability and address contributing illness or disordered eating; simply imposing withdrawal bleeds can conceal persisting energy deficiency. Hormone replacement may be appropriate for ovarian insufficiency, while thyroid, prolactin-related and anatomical disorders need their own pathways. Management of chronic anovulation includes reproductive goals and protection of the endometrium, rather than just the appearance of regular bleeding.^[ref][ref]