Clinical overview
The pathology of heavy menstrual bleeding (HMB) is the pathology of the FIGO PALM-COEIN causes. This chapter complements Heavy menstrual bleeding management by drilling into the histology and mechanism for each cause. Understanding the pathology is what turns the registrar from someone who follows a flowchart into someone who can predict which treatment will succeed and which is likely to fail.
Core knowledge
Structural PALM causes alter the endometrium or myometrium through polyps, adenomyosis, submucosal fibroids and hyperplasia.
Polyp (P)
Pathology:
- Localised endometrial overgrowth with fibrovascular stroma; covered by endometrial epithelium.
- Sessile or pedunculated.
- Glandular pattern within polyp may be inactive, functional, or hyperplastic; rarely malignant (<5% in postmenopausal symptomatic polyps; <1% in premenopausal).
Clinical correlate:
- HMB and IMB through ulceration of polyp surface, asynchronous bleeding from polyp tissue.
- Often asymptomatic; sometimes presents with PMB.
- Removed for symptoms or to exclude malignancy.
Adenomyosis (A)
Pathology:
- Endometrial glands and stroma within myometrium.
- Surrounded by smooth muscle hypertrophy; junctional zone disordered.
- Cyclical bleeding within myometrial islands → inflammation, fibrosis, microhaemorrhages.
- Disturbed myometrial contractility.
Clinical correlate:
- Bulky, tender, boggy uterus.
- HMB and dysmenorrhoea (progressive over years).
- Often misdiagnosed as fibroids. See Endometriosis pathophysiology for detail and MUSA criteria for diagnosis (Endometriosis staging).
Leiomyoma (L) — fibroids
Pathology:
- Monoclonal benign smooth muscle tumour.
- Whorled bundles of smooth muscle cells.
- Pseudocapsule of compressed adjacent myometrium.
- Variable vascularity; may undergo degenerations: hyaline (most common), cystic, red (in pregnancy — ischaemic), calcific, sarcomatous (rare, <0.5%).
- FIGO classification 0–8: 0 (pedunculated intracavitary) → 8 (extrauterine pedunculated).