Dysmenorrhea is painful menstrual cramping, typically caused by excessive prostaglandin-mediated uterine contractions (primary) or underlying pelvic pathology such as endometriosis or fibroids (secondary).

Dysmenorrhea

Dysmenorrhea is the most common gynaecological complaint and the leading cause of recurrent short-term school/work absenteeism in young women ^[1]
Prevalence: estimates vary from 45–95% of menstruating women depending on the population and definition used
- In Hong Kong, studies have found prevalence rates of approximately 50–80% among adolescents and young women
- Of these, approximately 10–20% describe it as severe (significantly limiting activities)
Primary dysmenorrhea: typically begins within 1–2 years of menarche (once ovulatory cycles are established) and peaks in the late teens to early 20s, with a tendency to improve with age and after childbirth ^[1]
Secondary dysmenorrhea: can begin at any age but more commonly presents in women > 25 years or in those with a history of initially pain-free periods that progressively worsen ^[1]

Risk Factors

For primary dysmenorrhea:

Younger age (< 30 years) — ovulatory cycles with high prostaglandin production
Earlier menarche (< 12 years) — longer cumulative exposure to prostaglandin-mediated pain cycles
Heavy menstrual flow (menorrhagia) — more endometrial tissue shed → more prostaglandin released
Nulliparity — the cervical os is relatively stenotic; after vaginal delivery, the os dilates, reducing resistance to menstrual flow (and hence less uterine contractility needed)
Family history — genetic component to prostaglandin sensitivity/production
Smoking — nicotine causes vasoconstriction → uterine ischaemia → worsens pain
Obesity — adipose tissue as an endocrine organ alters prostaglandin/oestrogen metabolism
Psychological factors — anxiety, depression, stress correlate with increased pain perception (central sensitisation)
Low physical activity — exercise ↑ endorphins which are natural analgesics

For secondary dysmenorrhea — essentially the risk factors for the underlying condition:

Endometriosis (most common cause of secondary dysmenorrhea) — nulliparity, family history, early menarche, short cycles
Adenomyosis — multiparous women, prior uterine surgery
Uterine fibroids (leiomyomata) — increasing age, African ethnicity, nulliparity, obesity ^[2]
Pelvic inflammatory disease (PID) — multiple sexual partners, STIs (Chlamydia, Gonorrhoea)
Intrauterine device (copper IUD) — a well-known cause of worsened dysmenorrhea
Endometrial polyps, cervical stenosis, uterine anomalies

High Yield

The classic exam question: "A 16-year-old girl with painful periods starting 18 months after menarche" → think primary dysmenorrhea. "A 35-year-old multiparous woman with progressively worsening painful, heavy periods" → think secondary dysmenorrhea (adenomyosis or endometriosis).

Anatomy and Function

Understanding dysmenorrhea requires a solid grasp of uterine anatomy and the menstrual cycle physiology.

Etiology and Pathophysiology

Primary dysmenorrhea is caused by excessive prostaglandin production by the endometrium during menstruation, leading to abnormally strong and prolonged uterine contractions and ischaemia. ^[1]

Step-by-step pathophysiology:

Progesterone withdrawal at the end of the luteal phase (corpus luteum regression if no pregnancy)
This leads to destabilization of endometrial cell membranes → activation of phospholipase A2
Phospholipase A2 cleaves arachidonic acid from membrane phospholipids
Arachidonic acid is metabolized by:
- Cyclooxygenase (COX-1 and COX-2) → Prostaglandins (PGF2α, PGE2) and Thromboxane A2
- Lipoxygenase → Leukotrienes (also contribute to pain and inflammation)
PGF2α is the key mediator:
- Potent stimulator of myometrial smooth muscle contraction → dysrhythmic, tonic contractions with elevated baseline uterine tone
- Vasoconstriction of spiral arteries → endometrial ischaemia
- The combination of high intrauterine pressure (sometimes exceeding arterial pressure, > 150–180 mmHg in severe cases) and vasoconstriction creates tissue ischaemia → pain
PGE2 contributes to:
- Pain sensitization — lowers the threshold of nociceptors
- Vasodilation in some vascular beds → contributes to associated symptoms like headache and flushing
Vasopressin may also play a role:
- Levels are elevated in women with dysmenorrhea
- Acts as an additional uterine muscle stimulant and vasoconstrictor
- May contribute to the "ischaemic" component of pain

Why only ovulatory cycles?

Anovulatory cycles do not produce a corpus luteum → no significant progesterone → no progesterone withdrawal → less organized secretory endometrium → less prostaglandin production
This is why primary dysmenorrhea typically begins 1–2 years after menarche (when ovulatory cycles become established) and why the combined oral contraceptive pill (COCP) — which suppresses ovulation — is an effective treatment

Supporting evidence:

Women with primary dysmenorrhea have been shown to have 2–7× higher endometrial prostaglandin levels compared to pain-free women
Menstrual fluid prostaglandin levels correlate with pain severity
NSAIDs (prostaglandin synthesis inhibitors) relieve dysmenorrhea in ~80% of women

Other contributing factors:

Leukotrienes (via the lipoxygenase pathway) — also contribute to myometrial contraction and may explain why ~20% of women do not respond to NSAIDs alone
Psychological/central factors: Central sensitization, catastrophising, and anxiety can amplify pain perception. There is overlap with other functional pain syndromes (e.g., IBS, fibromyalgia, chronic fatigue syndrome — note the association with dysmenorrhea mentioned in the IBS section) ^[3]
Cervical stenosis — a narrower cervical os may impede menstrual outflow → higher intrauterine pressure needed to expel menstrual debris → more pain (this partly explains why pain often improves after vaginal delivery)

Secondary dysmenorrhea has a structural/pathological cause. The pathophysiology depends on the specific etiology:

Etiology	Pathophysiology	Key Features
Endometriosis	Ectopic endometrial tissue (outside uterus) responds to cyclic hormones → bleeds → causes local inflammation, adhesions, fibrosis. Peritoneal irritation → pain. Also ↑ prostaglandin production locally.	Most common cause of secondary dysmenorrhea. Pain often starts before menses and continues throughout. Deep dyspareunia, dyschezia (painful defecation, if rectovaginal involvement), subfertility
Adenomyosis	Endometrial glands and stroma invade the myometrium → ectopic tissue bleeds cyclically within the muscle → local inflammation, muscular hypertrophy. Enlarged, boggy uterus contracts abnormally. Also ↑ local prostaglandin/cytokine production.	Classically in multiparous women > 35 years. Heavy, painful periods. Uterus is uniformly enlarged, globular, and tender ("boggy") on examination ^[2]
Uterine fibroids (leiomyomata) ^[2]	Benign smooth muscle tumours of the myometrium. Submucous fibroids distort the endometrial cavity → ↑ surface area → heavier bleeding; may also interfere with myometrial contraction (the uterus "tries" to expel the fibroid like a foreign body) → pain. Intramural fibroids may compress surrounding myometrium → altered contraction patterns. Fibroids that undergo red degeneration (haemorrhagic infarction, classically in pregnancy) cause acute pain.	May be asymptomatic. When symptomatic: menorrhagia (most common symptom), dysmenorrhea, pressure symptoms (urinary frequency, constipation), subfertility. ^[2]
Pelvic inflammatory disease (PID)	Ascending infection (commonly Chlamydia trachomatis, Neisseria gonorrhoeae) → endometritis, salpingitis, tubo-ovarian abscess → chronic inflammation, adhesions → chronic pelvic pain including dysmenorrhea	Dysmenorrhea + abnormal vaginal discharge, fever, cervical motion tenderness, adnexal tenderness
Copper intrauterine device (Cu-IUD)	Foreign body reaction → local inflammation → ↑prostaglandin production within the endometrium	Dysmenorrhea and menorrhagia typically worsen in the first 3–6 months after insertion
Endometrial polyps	Polyps protrude into the uterine cavity → irregular bleeding, and the uterus may contract to try to expel them	Intermenstrual bleeding, menorrhagia, postmenopausal bleeding
Cervical stenosis	Congenital or acquired (post-surgical, e.g., cone biopsy, LLETZ) narrowing of the cervical canal → obstructed menstrual outflow → ↑intrauterine pressure → pain	Scanty menstrual flow, severe cramping, possible haematometra
Uterine anomalies (e.g., bicornuate, septate uterus)	Obstructed outflow from one horn or abnormal myometrial architecture → dysmenorrhea	May present with primary dysmenorrhea but is technically a structural cause
Ovarian cysts/masses ^[2]	Functional cysts (follicular, corpus luteum) may cause cyclical pain if they bleed or undergo torsion. Endometriomas ("chocolate cysts") → cyclical pain due to bleeding within the cyst.	Ovarian cysts may present as pelvic mass ± pain. Endometriomas are strongly associated with endometriosis ^[2]

Hong Kong Context

In Hong Kong, the most important secondary causes to consider are endometriosis (common, often underdiagnosed, contributes to the significant subfertility burden), adenomyosis (increasing recognition with better imaging), and uterine fibroids (very common in Chinese women, with prevalence up to 20–40% in reproductive age). Copper IUD use is less prevalent in HK compared to some other regions (the levonorgestrel-releasing intrauterine system/Mirena is more commonly used and actually treats dysmenorrhea). PID is seen in sexually active young women, particularly in the context of STIs.

Classification

Grade	Description
Grade 0	Menstruation is not painful, daily activity unaffected
Grade 1 (Mild)	Menstruation is painful but seldom inhibits activity; analgesics rarely required
Grade 2 (Moderate)	Daily activity affected; analgesics required and provide relief; absent from work/school rarely
Grade 3 (Severe)	Activity clearly inhibited; analgesics provide poor relief; associated vegetative symptoms (nausea, vomiting, diarrhoea, headache); absenteeism from work/school

Clinical Features

A. Primary Dysmenorrhea

Symptom	Pathophysiological Basis
Crampy, spasmodic lower abdominal/suprapubic pain	PGF2α causes rhythmic myometrial contractions → intermittent ischaemia → visceral pain referred to T10–L1 dermatomes (lower abdomen/suprapubic area). Pain is "colicky" because contractions are rhythmic, not constant.
Pain begins with (or just before) onset of menstruation, lasting 1–3 days	Prostaglandin release is maximal in the first 48 hours of menstruation as the endometrium sheds; levels then decline.
Radiation to the lower back and medial thighs	Referred pain via the hypogastric plexus and presacral nerves to L2–L3 dermatomes (back) and via obturator nerve distribution (medial thigh).
Nausea and vomiting	Prostaglandins (esp. PGE2) enter the systemic circulation → stimulate the chemoreceptor trigger zone (CTZ) and smooth muscle of the GI tract → nausea/vomiting.
Diarrhoea and loose stools	PGF2α and PGE2 stimulate smooth muscle contraction throughout the GI tract → ↑ intestinal motility → diarrhoea. (This is also why IBS symptoms often worsen during menses.)
Headache	Systemic prostaglandin release → vasodilation of cerebral vessels → headache. Also possible prostaglandin-mediated central sensitization.
Fatigue, malaise, dizziness	Systemic effects of prostaglandins and vasopressin; also related to blood loss, sleep disturbance from pain, and stress.
Bloating	Prostaglandin-mediated changes in GI motility and fluid retention from hormonal fluctuations in the late luteal phase.

Temporal pattern of primary dysmenorrhea:

Onset: typically 1–2 years after menarche (once ovulatory cycles are established)
Pain begins within hours of onset of menstrual bleeding (or up to 1 day before)
Duration: usually 48–72 hours (corresponding to peak prostaglandin levels)
Tends to improve with age and after childbirth (cervical dilatation, altered prostaglandin production)

Sign	Pathophysiological Basis
Lower abdominal tenderness (suprapubic)	Reflects myometrial hypercontractility and visceral pain; tenderness is generally mild and diffuse, not localized
Normal bimanual pelvic examination	This is the key finding — by definition, primary dysmenorrhea has no identifiable pelvic pathology. The uterus is normal size, anteverted/anteflexed (typically), non-tender or only mildly tender, and adnexae are clear.
No cervical motion tenderness (chandelier sign negative)	Absence of pelvic infection or peritoneal irritation
No adnexal masses or tenderness	No ovarian pathology

Exam Pearl

A common mistake is to diagnose primary dysmenorrhea without performing a pelvic examination. Primary dysmenorrhea is a diagnosis of exclusion — you must confirm normal pelvic findings. If there are abnormal findings (enlarged uterus, adnexal mass, cervical motion tenderness, nodularity in the pouch of Douglas), you are dealing with secondary dysmenorrhea and must investigate further.

B. Secondary Dysmenorrhea

The clinical features depend on the underlying cause. However, there are features that should raise suspicion for secondary dysmenorrhea over primary:

Feature	Why It Suggests Secondary Cause
Onset after age 25 or new-onset dysmenorrhea in a woman who previously had painless periods	Primary dysmenorrhea begins in adolescence; late onset suggests new pathology developing
Progressive worsening of pain over time	Primary dysmenorrhea tends to stay stable or improve; progressive worsening suggests evolving pathology (e.g., enlarging endometrioma, growing fibroid, worsening adenomyosis)
Pain starting > 1–2 days before menstruation and/or persisting beyond day 3	Primary dysmenorrhea pain is closely temporally linked to menstrual flow (prostaglandin release); pain that precedes flow by several days suggests endometriosis (pre-menstrual peritoneal inflammation)
Heavy menstrual bleeding (menorrhagia) or irregular bleeding	Suggests fibroids, adenomyosis, or endometrial polyps
Deep dyspareunia (pain with deep penetration during intercourse)	Suggests endometriosis (especially involving the uterosacral ligaments or pouch of Douglas) or adenomyosis
Dyschezia (painful defecation, especially during menses)	Suggests endometriosis involving the rectovaginal septum or bowel
Dysuria during menses	Suggests bladder endometriosis
Subfertility	Endometriosis is a leading cause of subfertility
Abnormal vaginal discharge	Suggests PID
Failure to respond to NSAIDs and/or COCP	Most women with primary dysmenorrhea respond to first-line therapy; non-response should prompt investigation for secondary causes

Endometriosis:

Symptoms: Cyclical pelvic pain (often pre-menstrual onset), deep dyspareunia, dyschezia, dysuria, subfertility, chronic pelvic pain
Signs: Tender nodularity in the pouch of Douglas (felt on rectovaginal examination), fixed retroverted uterus (due to adhesions), visible blue/brown lesions on the posterior vaginal fornix or cervix (occasionally)
Pathophysiology: Ectopic endometrial-like tissue implants respond to oestrogen → cyclical proliferation, bleeding → local inflammation, fibrosis, adhesion formation, and nociceptor activation. Also ↑ local prostaglandin, cytokine, and growth factor production.

Adenomyosis: ^[2]

Symptoms: Dysmenorrhea (progressively worsening), menorrhagia, chronic pelvic pain
Signs: Uniformly enlarged, globular, "boggy" tender uterus (typically 2–3× normal size, rarely > 12 weeks' size), often symmetrically enlarged (vs. the irregular enlargement of fibroids)
Pathophysiology: Endometrial glands and stroma within the myometrium → cyclic bleeding into the muscle → smooth muscle hypertrophy and hyperplasia around the ectopic foci → altered contractility, ↑ prostaglandin production locally

Uterine fibroids: ^[2]

Symptoms: Menorrhagia (most common symptom), dysmenorrhea (esp. with submucous fibroids), pressure symptoms (urinary frequency if anterior, constipation if posterior, ureteric obstruction if lateral), abdominal distension with large fibroids
Signs: Irregularly enlarged, firm, non-tender uterus with palpable discrete lumps (fibroids); may be palpable abdominally if large (> 12 weeks' size)
Fibroids are oestrogen- and progesterone-dependent → grow during reproductive years, may shrink after menopause ^[2]
Types by location: subserosal, intramural, submucosal (most symptomatic for bleeding/pain), pedunculated, cervical ^[2]
Pathophysiology of pain: submucosal fibroids distort the cavity → ↑ surface area → ↑ bleeding; also, the uterus contracts to try to expel the fibroid (similar to labour contractions → colicky pain). Intramural fibroids may compress vessels → ischaemia.

Pelvic inflammatory disease (PID):

Symptoms: Lower abdominal pain (may be constant, not just menstrual), abnormal vaginal discharge (purulent, foul-smelling), intermenstrual or post-coital bleeding, dyspareunia, fever
Signs: Cervical motion tenderness (chandelier sign positive), adnexal tenderness ± mass (tubo-ovarian abscess), fever, mucopurulent cervicitis
Pathophysiology: Ascending infection → endometritis → salpingitis → chronic inflammation and adhesions → chronic pelvic pain and dysmenorrhea

Feature	Primary	Secondary
Age of onset	1–2 years after menarche (teens)	Usually > 25 years or later onset
Temporal pattern	Starts with/just before menses, lasts 1–3 days	May begin days before menses, persist after menses ends
Progression	Stable or improving over time	Progressive worsening
Pelvic examination	Normal	Abnormal findings (enlarged uterus, nodularity, masses, tenderness)
Associated features	GI symptoms (nausea, diarrhoea), headache	Menorrhagia, dyspareunia, dyschezia, subfertility, discharge
Response to NSAIDs/COCP	Usually good (~80%)	Variable; poor response should prompt investigation
Menstrual flow	Normal	Often heavy or irregular

High Yield Summary

Definition: Dysmenorrhea = painful menstruation. Primary = no pelvic pathology; Secondary = underlying cause present.

Epidemiology: Most common gynaecological complaint; affects 45–95% of menstruating women. Primary peaks in teens-20s; secondary more common > 25 years.

Pathophysiology of Primary Dysmenorrhea: Progesterone withdrawal → phospholipase A2 → arachidonic acid → COX → PGF2α + PGE2 → myometrial hypercontractility + spiral artery vasoconstriction → uterine ischaemia → pain. Only occurs in ovulatory cycles.

Key Risk Factors: Young age, early menarche, heavy flow, nulliparity, smoking, family history, low physical activity.

Key Clinical Features of Primary: Crampy suprapubic pain beginning with menses (lasts 48–72h), ± nausea/vomiting/diarrhoea/headache, normal pelvic exam.

Red Flags for Secondary: Late onset, progressive worsening, pain before/after menses, menorrhagia, dyspareunia, dyschezia, subfertility, abnormal pelvic exam, failure to respond to NSAIDs/COCP.

Top 3 Secondary Causes in HK: (1) Endometriosis, (2) Adenomyosis, (3) Uterine fibroids.

Associations: Dysmenorrhea is associated with IBS, fibromyalgia, and other functional pain syndromes (shared prostaglandin/central sensitization pathways).

Active Recall - Dysmenorrhea (Definition to Clinical Features)

Differential Diagnosis of Dysmenorrhea

When a woman presents with painful menstruation, the clinical task is twofold: (1) Is this primary or secondary dysmenorrhea? and (2) If secondary, what is the underlying cause? But more broadly, you must also consider non-gynaecological causes of cyclical or chronic pelvic pain that can masquerade as or coexist with dysmenorrhea. Think of dysmenorrhea not just as a diagnosis but as a symptom — and approach it the way you would any pelvic pain, with a systematic differential.

A. Gynaecological Causes

B. Non-Gynaecological Causes

These are important because they can mimic or coexist with dysmenorrhea and are easily missed if you have "tunnel vision" on gynaecological causes.

Condition	Why It Mimics Dysmenorrhea	Distinguishing Features
Irritable bowel syndrome (IBS)	IBS symptoms (crampy abdominal pain, bloating, altered bowel habit) frequently worsen during menstruation due to prostaglandin effects on GI smooth muscle. IBS is associated with dysmenorrhea ^[3]. Shared pathophysiology: visceral hypersensitivity, central sensitisation.	Pain associated with defecation (improves or worsens with bowel movements); altered bowel habit (diarrhoea, constipation, or mixed); bloating prominent; meets Rome IV criteria
Inflammatory bowel disease (IBD) — Crohn's, UC	Chronic pelvic/abdominal pain may flare cyclically; bowel endometriosis can mimic IBD	Bloody diarrhoea (UC), right iliac fossa pain (Crohn's), weight loss, extra-intestinal manifestations, raised inflammatory markers
Appendicitis	Acute right iliac fossa pain can overlap with right-sided ovarian pathology or dysmenorrhea	Migratory pain (periumbilical → RIF), anorexia, fever, RIF tenderness with guarding, elevated WCC/CRP; acute onset, not cyclical ^[4]^[6]

IBS and Dysmenorrhea — A Common Overlap

Up to 50% of women with IBS report worsening of GI symptoms during menstruation, and women with dysmenorrhea have higher rates of IBS. This makes clinical sense: prostaglandins released during menstruation stimulate smooth muscle contraction throughout the body, including the bowel. Additionally, both conditions involve visceral hypersensitivity — a lowered threshold for pain perception in hollow viscera. Always ask about bowel symptoms in a woman presenting with dysmenorrhea, and ask about menstrual pain in a woman presenting with IBS ^[3].

Condition	Why It Mimics Dysmenorrhea	Distinguishing Features
Interstitial cystitis / Painful bladder syndrome	Chronic suprapubic/pelvic pain that may worsen with menses (hormonal influence on bladder mucosa); coexists with dysmenorrhea and IBS in many women	Pain related to bladder filling, relieved by voiding; urinary frequency and urgency (often > 8×/day); absence of infection on MSU; diagnosis of exclusion ^[7]
UTI / Cystitis	Suprapubic pain, dysuria	Storage LUTS (frequency, urgency, dysuria), turbid/bloody urine, positive urine dipstick/culture ^[7]
Ureteric colic	Acute loin-to-groin pain can overlap with pelvic pain	Colicky pain that waxes and wanes (20–60 min episodes), loin tenderness, haematuria, history of renal stones ^[7]

Condition	Why It Mimics Dysmenorrhea	Distinguishing Features
Myofascial pelvic pain / Pelvic floor dysfunction	Trigger points in pelvic floor muscles can cause chronic pelvic pain that may worsen with menses (hormonal effects on muscle tone)	Tender trigger points on pelvic floor examination; pain reproduced by palpation of specific muscles; not temporally linked to menstrual flow per se
Musculoskeletal back pain	Lower back pain can be confused with the back component of dysmenorrhea	Not cyclical, related to movement/posture, no suprapubic component, no menstrual timing

Condition	Why It Mimics Dysmenorrhea	Distinguishing Features
Somatoform/somatic symptom disorder	Chronic pelvic pain without identifiable cause; ≥1 somatic symptom a/w distress and/or functional impairment; excessive thoughts/anxiety about symptoms ^[8]	Multiple somatic symptoms across organ systems, persistent (≥6 months), excessive health-related anxiety, functional impairment disproportionate to findings; diagnosis of exclusion after thorough workup
Central sensitisation / Chronic pelvic pain syndrome	After prolonged nociceptive input (e.g., from chronic endometriosis), the CNS can undergo central sensitisation → pain persists even after the original cause is treated	Pain persists despite adequate treatment of identifiable cause; widespread tenderness; often coexists with fibromyalgia, IBS, chronic fatigue

Don't Forget These Non-Gynaecological Mimics

A common exam and clinical mistake is to attribute all pelvic pain in a menstruating woman to dysmenorrhea without considering the GI, urological, and musculoskeletal differentials. Appendicitis, ectopic pregnancy, and ovarian torsion are surgical emergencies that present with acute pelvic pain. Always ask about bowel symptoms, urinary symptoms, and pregnancy in your history. Always do a pregnancy test.

History and physical examination usually help to suggest a diagnosis ^[5].

The following table summarises the key historical and examination features that help narrow the differential:

Feature	Favours Primary	Favours Secondary	Specific Cause Suggested
Age of onset	Adolescent (1–2y post-menarche)	> 25 years or new-onset in previously pain-free woman	—
Temporal pattern	Pain starts with menses, lasts ≤ 3 days	Pain starts days before menses, persists after	Pre-menstrual onset → endometriosis
Progression	Stable or improving	Progressive worsening	Endometriosis, adenomyosis, growing fibroid
Menstrual flow	Normal	Heavy (menorrhagia)	Fibroids, adenomyosis, polyps, Cu-IUD
Dyspareunia	Absent	Deep dyspareunia	Endometriosis, adenomyosis
Dyschezia	Absent	Painful defecation during menses	Rectovaginal endometriosis
Subfertility	Absent	Present	Endometriosis, PID (tubal damage)
Vaginal discharge	Absent	Abnormal/purulent discharge	PID
Fever	Absent	Present	PID, tubo-ovarian abscess, torsion with necrosis
Pelvic exam	Normal	Abnormal	See below
Response to NSAIDs/COCP	Good (80%)	Poor	Consider secondary cause if non-responsive
Pregnancy test	Negative	Positive	Ectopic pregnancy

Examination findings pointing to specific diagnoses:

Examination Finding	Suggested Diagnosis
Normal pelvic examination	Primary dysmenorrhea
Uniformly enlarged, globular, boggy, tender uterus	Adenomyosis ^[2]
Irregularly enlarged, firm uterus with discrete lumps	Uterine fibroids ^[2]
Tender nodularity in pouch of Douglas	Endometriosis
Fixed, retroverted uterus	Endometriosis (adhesions)
Cervical motion tenderness + adnexal tenderness	PID or ectopic pregnancy
Adnexal mass	Ovarian cyst, endometrioma, ectopic pregnancy, tubo-ovarian abscess ^[2]
Absent/scanty menstrual flow with severe pain	Cervical stenosis, outflow obstruction

Category	Condition	Key Differentiating Feature
Primary	Primary dysmenorrhea	Normal pelvic exam, onset in adolescence, responds to NSAIDs/COCP
Secondary — Uterine	Adenomyosis	Multiparous, > 35y, boggy tender uterus, menorrhagia
	Uterine fibroids	Irregular firm uterus, menorrhagia, pressure symptoms
	Endometrial polyps	Intermenstrual/irregular bleeding
	Cervical stenosis	Scanty flow, severe cramping, Hx of cervical procedure
	Cu-IUD	Temporal relationship with IUD insertion
	Uterine anomalies	Severe from menarche, non-responsive, associated renal anomalies
Secondary — Ovarian/Adnexal	Endometriosis	Pre-menstrual pain, dyspareunia, dyschezia, subfertility, nodularity in POD
	Ovarian cyst complications	Acute onset, unilateral, ± nausea/vomiting (torsion)
	Mittelschmerz	Mid-cycle, unilateral, self-limiting
Secondary — Pelvic	PID	Bilateral pain, discharge, fever, cervical motion tenderness
	Adhesions	History of surgery/PID/endometriosis, chronic pain
	Ectopic pregnancy	Positive pregnancy test, missed period, adnexal pain, spotting
Non-gynae — GI	IBS	Bowel symptoms, Rome IV criteria, worsens with menses
	IBD	Bloody diarrhoea, weight loss, raised CRP
	Appendicitis	Acute, migratory RIF pain, fever, peritonism
Non-gynae — Urological	Interstitial cystitis	Bladder pain related to filling, frequency, no infection
	UTI	Dysuria, frequency, urgency, positive MSU
	Ureteric colic	Colicky loin-to-groin pain, haematuria
Non-gynae — Other	Myofascial pelvic pain	Trigger points, not cyclical
	Somatoform disorder	Multiple unexplained symptoms, excessive health anxiety

High Yield Summary

Most common cause of dysmenorrhea overall: Primary dysmenorrhea (diagnosis of exclusion — normal pelvic exam required).

Most common cause of secondary dysmenorrhea: Endometriosis.

Top gynaecological differentials for secondary dysmenorrhea: Endometriosis, adenomyosis, uterine fibroids, PID, ovarian cysts.

Non-gynaecological mimics to never forget: IBS (very common overlap), interstitial cystitis, appendicitis, ectopic pregnancy (always do a pregnancy test!).

Red flags for secondary cause: Late onset, progressive worsening, pre-menstrual pain onset, menorrhagia, dyspareunia, dyschezia, subfertility, abnormal exam, failure of NSAIDs/COCP.

Emergency differentials in acute pelvic pain: Ectopic pregnancy (ruptured), ovarian torsion, ruptured ovarian cyst, PID/tubo-ovarian abscess, appendicitis — these are time-critical and must be excluded before attributing pain to dysmenorrhea.

Classify pelvic mass differentials into: gynaecological (uterine vs. ovarian) and non-gynaecological (GI, urological, retroperitoneal) ^[1]^[2]^[5].

Active Recall - Differential Diagnosis of Dysmenorrhea

References

^[1] Lecture slides: GC 114. Climacteric symptoms menopause and related illness; amenorrhoea.pdf ^[2] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf; GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[3] Senior notes: Ryan Ho GI.pdf (Section 3.2.1 — Irritable Bowel Syndrome, association with dysmenorrhea) ^[4] Lecture slides: Block C - Gyanecological Emergency Notes to Students.pdf ^[5] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (Summary slide) ^[6] Senior notes: Ryan Ho GI.pdf (Section on differential diagnoses in adult females — PID, ovarian cyst complications, ectopic pregnancy, Mittelschmerz) ^[7] Senior notes: Ryan Ho Urogenital.pdf (Section 6.1 — Approach to Dysuria; interstitial cystitis) ^[8] Senior notes: Ryan Ho Psychiatry.pdf (Section 8.4 — Somatoform Disorders)

Diagnostic Criteria, Algorithm, and Investigations for Dysmenorrhea

Diagnostic Criteria

Dysmenorrhea does not have formal "diagnostic criteria" in the way that, say, rheumatoid arthritis or SLE does with scored classification systems. Instead, the diagnosis is made clinically based on the pattern of symptoms and the presence or absence of underlying pathology. Let's break this down for primary and secondary dysmenorrhea.

Investigation Modalities

Investigations for dysmenorrhea are selected based on clinical findings. Primary dysmenorrhea requires no investigations if the history is classic, examination is normal, and the patient responds to empirical therapy. Investigations are directed at identifying secondary causes.

Test	Rationale	Key Findings & Interpretation
Full blood count (CBC)	Anaemia related to menorrhagia ^[1] — if a woman has heavy periods alongside dysmenorrhea (fibroids, adenomyosis), she may develop iron deficiency anaemia	↓ Hb, ↓ MCV (microcytic), ↓ ferritin = iron deficiency anaemia from chronic blood loss. Why microcytic? Iron is needed for haem synthesis → less haemoglobin per red cell → cells are smaller
Iron studies (ferritin, serum iron, TIBC)	To confirm iron deficiency if anaemia is present	↓ Ferritin (most sensitive early marker of iron depletion), ↓ serum iron, ↑ TIBC (the body upregulates transferrin production to try to capture more iron)
CRP / ESR	If PID is suspected (fever, discharge, cervical motion tenderness)	↑ CRP/ESR suggests active infection/inflammation. However, these are non-specific
Urine pregnancy test (β-hCG)	To exclude pregnancy, especially ectopic pregnancy — this is mandatory in any reproductive-age woman with acute pelvic pain	Positive → manage as pregnancy (confirm intrauterine vs. ectopic with TVS). Negative → proceed with other workup
STI screening (endocervical/vaginal swabs)	If PID is suspected: Chlamydia trachomatis NAAT, Neisseria gonorrhoeae NAAT, high vaginal swab for Trichomonas, Gardnerella	Positive NAAT for Chlamydia/Gonorrhoea confirms sexually transmitted aetiology of PID → treat with appropriate antibiotics and contact trace

These are not routinely required for dysmenorrhea but are indicated in specific scenarios:

Test	When Indicated	Key Findings & Interpretation
FSH, LH, E2, PRL, TFT, testosterone ^[9]	When dysmenorrhea is associated with amenorrhoea, oligomenorrhoea, or features of hyperandrogenism (suggesting PCOS, premature ovarian insufficiency, thyroid disease, or hyperprolactinaemia)	↑ LH:FSH ratio ( > 2:1) + ↑ testosterone → PCOS. ↑ FSH + ↓ E2 → premature ovarian insufficiency. ↑ PRL → prolactinoma (can cause amenorrhoea/oligomenorrhoea). ↑/↓ TSH → thyroid disease
Androgens (SHBG, 17-OH progesterone) ^[9]	If PCOS or congenital adrenal hyperplasia suspected	↓ SHBG (insulin resistance in PCOS drives hepatic SHBG production down → more free androgens). ↑ 17-OHP → congenital adrenal hyperplasia (21-hydroxylase deficiency)
CA-125	Sometimes measured when an ovarian mass is found, to help differentise benign vs. malignant; also mildly elevated in endometriosis and adenomyosis	Not diagnostic for endometriosis — sensitivity is poor and specificity is low. May be ↑ in endometriosis (typically < 200 U/mL), ovarian cancer (often > 200), PID, fibroids, pregnancy, menses itself. Not a screening tool — only useful in the context of a pelvic mass to guide further management ^[2]

CA-125 in Dysmenorrhea

CA-125 is frequently over-ordered. It is not a screening test for endometriosis, and it can be elevated during normal menstruation. In the context of dysmenorrhea, its main utility is when an ovarian mass is identified on ultrasound and you need to assess malignancy risk (using the Risk of Malignancy Index — RMI). A mildly elevated CA-125 in a young woman with dysmenorrhea is more likely to reflect endometriosis, menstruation, or even the investigation itself rather than cancer ^[2].

Pelvic ultrasound is commonly performed ^[5] and is the first-line imaging investigation for suspected secondary dysmenorrhea.

Two approaches:

Modality	Description	Advantages	Limitations
Transvaginal ultrasound (TVS)	High-frequency probe inserted into the vagina, providing high-resolution images of the uterus, ovaries, and pouch of Douglas	Best resolution for pelvic organs — superior for detecting fibroids, adenomyosis, ovarian cysts, endometriomas, and assessing endometrial thickness. Can assess uterine anomalies. Doppler flow can assess vascularity of masses	Requires patient consent (may not be appropriate for adolescents who are not sexually active); limited field of view for large masses
Transabdominal ultrasound (TAS)	Probe placed on the abdomen with a full bladder as an acoustic window	Non-invasive, appropriate for adolescents and those who decline TVS; good overview of large pelvic masses	Lower resolution for pelvic organs compared to TVS

Key ultrasound findings and their interpretation:

Condition	Ultrasound Findings	Why It Looks This Way
Uterine fibroids	Well-circumscribed hypoechoic round masses within the myometrium with whorled appearance. May show calcification (echogenic foci with posterior acoustic shadowing). Classified by location relative to endometrium and serosa. Fibroids have a pseudo-capsule surrounding it ^[1] — appears as a clear boundary on USS	Smooth muscle cells arranged in whorls → hypoechoic. Pseudo-capsule of compressed myometrium creates a distinct border. Calcification occurs in degenerated long-standing fibroids. Submucosal fibroids distort the endometrial stripe
Adenomyosis	Diffusely enlarged, globular uterus with heterogeneous myometrial echotexture ("Venetian blind" appearance = linear striations). Myometrial cysts (small anechoic areas) within the myometrium. Poorly defined endo-myometrial junction (junctional zone > 12 mm on MRI). Adenomyosis does not have a pseudo-capsule ^[1] → no distinct boundary between adenomyotic tissue and normal myometrium	Ectopic endometrial glands/stroma scattered through the myometrium disrupt the normal homogeneous muscle texture. Myometrial cysts represent dilated ectopic endometrial glands filled with old blood. Unlike fibroids, there is no compressed capsule — the disease infiltrates diffusely
Endometrioma ("chocolate cyst")	Homogeneous low-level internal echoes ("ground glass" appearance) within a well-defined ovarian cyst. No internal vascularity on Doppler. May have dependent layering	Old blood (haemolysed RBCs and haemosiderin) creates a dense, homogeneous fluid that produces the characteristic ground-glass echogenicity. "Chocolate" colour grossly due to degraded haemoglobin
Simple ovarian cyst	Anechoic (completely black), thin smooth wall, no internal septae, no solid component, posterior acoustic enhancement	Simple fluid (transudate) transmits sound waves uniformly → anechoic. No solid tissue → benign features
Complex ovarian cyst / mass	Internal septae, solid components, irregular walls, papillary projections, vascularity on Doppler	Solid components and papillary projections suggest neoplastic tissue. Increased vascularity suggests active growth. Features raise concern for malignancy → further workup with CA-125, RMI, +/- MRI, +/- refer to gynaecological oncology ^[2]
PID / Tubo-ovarian abscess	Thickened, fluid-filled fallopian tubes (hydrosalpinx/pyosalpinx — "cogwheel sign" on cross-section). Complex adnexal mass with thick walls. Free fluid in pouch of Douglas	Inflamed, pus-filled tubes lose their normal thin wall and become distended. Complex mass represents walled-off abscess with inflammatory debris
Uterine anomaly	3D USS can delineate the external uterine contour and the cavity shape — e.g., septate uterus shows a single external contour with a divided cavity; bicornuate shows a fundal indentation with two cavities	The fusion (or failure thereof) of the Müllerian ducts during embryological development determines the type of anomaly. 3D USS is superior to 2D for classification
Cervical stenosis / Haematometra	Distended uterine cavity filled with echogenic material (old blood), with a narrow or absent cervical canal	Obstructed outflow → menstrual blood accumulates → uterine cavity distends

Modality	When Indicated	Key Findings
MRI pelvis	Gold standard for adenomyosis — when USS is equivocal. Also excellent for deep infiltrating endometriosis, uterine anomaly delineation, and fibroid mapping (pre-surgical planning). 3D USG pelvis / MRI indicated for suspected anomalies ^[9]	Adenomyosis on MRI: junctional zone thickness > 12 mm (the junctional zone is the innermost layer of myometrium, appears as a dark band on T2-weighted MRI — in adenomyosis, this zone is thickened and irregular). Adenomyosis cannot be enucleated like fibroids ^[1] because there is no capsule — MRI shows the diffuse, ill-defined nature of the disease. Deep endometriosis on MRI: nodular lesions in the rectovaginal septum, uterosacral ligaments, or bladder wall — T1 hyperintense (blood products), T2 hypointense (fibrosis). Fibroids on MRI: well-circumscribed T2-hypointense masses (densely packed smooth muscle has low water content)
CT pelvis	Not first-line for gynaecological pathology due to poor soft tissue contrast (compared to MRI) and radiation exposure. May be done in emergency settings to exclude other causes of acute abdomen (e.g., appendicitis, perforation)	Incidental finding of uterine enlargement, calcified fibroids, or ovarian masses. CT is inferior to USS/MRI for characterising gynaecological pathology
Hysterosalpingography (HSG)	When subfertility is a concern alongside dysmenorrhea — assesses tubal patency and cavity contour	Tubal blockage (suggests PID/adhesions). Filling defects in the cavity (submucous fibroid, polyp). Abnormal cavity shape (uterine anomaly)

Modality	When Indicated	Key Findings
Diagnostic laparoscopy	Gold standard for diagnosis of endometriosis — indicated when there is strong clinical suspicion but USS/MRI is negative or equivocal, and/or when medical therapy has failed. Also allows for concurrent therapeutic intervention (excision/ablation of endometriotic lesions, adhesiolysis) ^[9]	Endometriotic implants: powder-burn (dark brown/black) lesions, red flame-like lesions (early active), white scarred lesions (old, fibrotic), peritoneal windows. Endometriomas: "chocolate cysts" on the ovary. Adhesions: filmy or dense, distorting anatomy. Staging: revised American Society for Reproductive Medicine (rASRM) classification (Stage I–IV based on implant location, depth, adhesion extent)
Hysteroscopy	When intrauterine pathology is suspected — submucous fibroids, endometrial polyps, uterine septum, cervical stenosis. Can be diagnostic and therapeutic.	Direct visualisation of the uterine cavity: submucous fibroids appear as smooth, well-circumscribed protrusions into the cavity; polyps appear as smooth, glistening, pedunculated growths; septum appears as a midline fibrous band
Endometrial biopsy / Pipelle sampling	When abnormal uterine bleeding coexists with dysmenorrhea, especially in women > 40 years or with risk factors for endometrial hyperplasia/cancer	Histology: normal secretory endometrium (primary dysmenorrhea); chronic endometritis (PID — plasma cells in the stroma); endometrial hyperplasia or malignancy (in older women with AUB)

Investigation	When Indicated	Key Findings
Urine microscopy, culture, and sensitivity (MSU)	If urinary symptoms coexist (dysuria, frequency) — to exclude UTI	Pyuria + bacteriuria → UTI. Sterile pyuria → consider Chlamydia urethritis or interstitial cystitis
Stool studies	If GI symptoms are prominent (to differentiate IBS from IBD)	Faecal calprotectin > 50 μg/g suggests intestinal inflammation (IBD rather than IBS)
Karyotype ^[9]	If primary amenorrhoea coexists with apparent dysmenorrhea/haematometra — to exclude chromosomal abnormalities (e.g., Turner syndrome mosaicism)	45,X or mosaic → Turner syndrome. 46,XY → androgen insensitivity syndrome or Swyer syndrome (won't typically have dysmenorrhea as there is no functioning endometrium)
Autoimmune screening ^[9]	If premature ovarian insufficiency is suspected (oligomenorrhoea/amenorrhoea + dysmenorrhea in young woman)	Anti-adrenal, anti-ovarian, anti-thyroid antibodies — autoimmune oophoritis as a cause of POI

Clinical Scenario	Investigation Strategy
Classic primary dysmenorrhea in adolescent	Pregnancy test (if sexually active). No further investigations needed if history and exam are classic. Trial of NSAIDs ± COCP. Investigate only if non-responsive after 3–6 months
Suspected endometriosis	Pregnancy test → Pelvic USS (TVS) → look for endometriomas, adenomyosis, other pelvic pathology. If USS is normal but clinical suspicion remains → MRI pelvis. If still equivocal or medical therapy fails → diagnostic laparoscopy (gold standard)
Suspected fibroids	Pelvic USS (TVS ± TAS) — sufficient for diagnosis in most cases. CBC (for anaemia from menorrhagia). MRI if surgical planning needed (fibroid mapping) or if differentiation from adenomyosis or sarcoma is required
Suspected adenomyosis	Pelvic USS (TVS) — look for features described above. If equivocal → MRI pelvis (gold standard). Note: definitive diagnosis is histological (from hysterectomy specimen), but clinical + imaging diagnosis is usually sufficient to guide management
Suspected PID	Pregnancy test, endocervical swabs (Chlamydia/Gonorrhoea NAAT), high vaginal swab, CBC, CRP. Pelvic USS if tubo-ovarian abscess suspected. Laparoscopy if diagnosis uncertain
Associated subfertility	Hormonal profile (FSH, LH, E2, PRL, TFT, testosterone, AMH). Pelvic USS. HSG or HyCoSy (tubal patency). Diagnostic laparoscopy if endometriosis suspected
Adolescent with severe dysmenorrhea from menarche, non-responsive to treatment	Think structural anomalies ^[1]. Pelvic USS (TAS if not sexually active). 3D USS or MRI to delineate Müllerian anatomy ^[9]. ± Examination under anaesthesia if vaginal anomaly suspected

High Yield Summary

Primary dysmenorrhea is a clinical diagnosis of exclusion — classic history + normal pelvic exam + response to NSAIDs/COCP. No investigations required in straightforward cases.

Mandatory investigation: Pregnancy test in any reproductive-age woman with pelvic pain.

First-line imaging: Pelvic ultrasound (TVS preferred for resolution; TAS for adolescents/those declining TVS). Pelvic ultrasound is commonly performed ^[5].

Gold standard for adenomyosis: MRI pelvis (junctional zone > 12 mm). Adenomyosis has no pseudo-capsule, unlike fibroids ^[1] — this is why it cannot be enucleated and appears ill-defined on imaging.

Gold standard for endometriosis: Diagnostic laparoscopy with direct visualisation and biopsy. USS/MRI may be normal in superficial peritoneal disease.

Trigger for investigation: Red flags for secondary cause, failure to respond to 3–6 months of empirical therapy, associated menorrhagia/subfertility/pelvic mass.

Key USS findings: Fibroids = well-circumscribed hypoechoic masses with pseudo-capsule; Adenomyosis = diffusely enlarged globular uterus with heterogeneous myometrium and myometrial cysts, no pseudo-capsule; Endometrioma = ground-glass ovarian cyst.

Hormonal workup (FSH, LH, E2, PRL, TFT, testosterone) is indicated when dysmenorrhea coexists with amenorrhoea/oligomenorrhoea, not for isolated dysmenorrhea.

Active Recall - Diagnostic Criteria, Algorithm, and Investigations for Dysmenorrhea

References

^[1] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[4] Lecture slides: Block C - Gyanecological Emergency Notes to Students.pdf ^[5] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (Summary slide) ^[9] Lecture slides: GC 114. Climacteric symptoms menopause and related illness; amenorrhoea.pdf

Management of Dysmenorrhea

The management of dysmenorrhea is fundamentally guided by whether you are dealing with primary or secondary dysmenorrhea. For primary, the approach is stepwise: lifestyle → NSAIDs → hormonal therapy → consider secondary causes if refractory. For secondary, you treat the underlying cause alongside symptom control. Let me walk you through this systematically.

A. Management of Primary Dysmenorrhea

These are often underestimated but have genuine physiological rationale. They should be offered to all women as first-line or adjunctive measures.

Measure	Mechanism / Rationale	Evidence
Regular exercise	Aerobic exercise ↑ endorphin release (endogenous opioids that raise pain threshold); ↑ pelvic blood flow → ↓ ischaemia; ↓ stress and anxiety (which amplify pain perception via central sensitisation)	Multiple RCTs show moderate benefit; recommended by ACOG and NICE
Local heat application (heating pad, hot water bottle to lower abdomen)	Heat causes smooth muscle relaxation and vasodilation → ↓ myometrial spasm and ↓ ischaemia. Heat also activates thermoreceptors that compete with nociceptive signals at the spinal cord level (gate control theory of pain)	RCTs show topical heat (40°C) is as effective as ibuprofen for pain relief
Dietary modification	Low-fat, plant-based diets may ↓ circulating oestrogen → ↓ endometrial prostaglandin production. Omega-3 fatty acids (fish oil) compete with arachidonic acid as COX substrate → ↓ pro-inflammatory prostaglandin synthesis (produces less potent PGE3 instead of PGE2)	Modest evidence; can be recommended as adjunctive
Stress management and psychological support	Anxiety and stress → central sensitisation and ↓ pain threshold. Cognitive behavioural therapy (CBT) and relaxation techniques can modify pain perception	Evidence limited but rationale is sound; particularly useful in those with comorbid anxiety/depression
Acupuncture and TENS	Transcutaneous electrical nerve stimulation (TENS): electrical impulses stimulate large-diameter Aβ fibres → inhibit pain transmission by small C-fibres at the dorsal horn (gate control theory). Acupuncture may work via endorphin release	Some evidence for TENS; acupuncture evidence is mixed
Smoking cessation	Nicotine causes vasoconstriction → ↑ uterine ischaemia → ↑ pain. Smoking also associated with higher circulating prostaglandin levels	Epidemiological data supports this; should be advised

NSAIDs ("Non-Steroidal Anti-Inflammatory Drugs") are the cornerstone of primary dysmenorrhea treatment. The name tells you the mechanism: they reduce inflammation without being steroids.

Why do NSAIDs work in dysmenorrhea?

NSAIDs inhibit cyclooxygenase (COX) enzymes → ↓ conversion of arachidonic acid to prostaglandins (PGF2α and PGE2)
This directly addresses the core pathophysiology: ↓ prostaglandin production → ↓ myometrial contractility → ↓ uterine ischaemia → ↓ pain
Also ↓ the systemic effects of prostaglandins (nausea, diarrhoea, headache)
Effective in ~80% of women with primary dysmenorrhea

Drug	Dose	Notes
Ibuprofen	400–600 mg TDS (max 2400 mg/day)	Most commonly used; good evidence base; available OTC
Naproxen	250–500 mg BD (max 1250 mg/day on day 1, then 1000 mg/day)	Longer half-life → less frequent dosing; good for women who forget midday dose
Mefenamic acid (Ponstan)	500 mg TDS	A fenamate — has additional direct anti-prostaglandin receptor activity (blocks prostaglandin action at the receptor level in addition to inhibiting synthesis). Popular choice in HK/UK for dysmenorrhea
Diclofenac	50 mg TDS or 75 mg BD	Effective; available in suppository form for those with nausea/vomiting
Celecoxib (COX-2 selective)	200 mg BD	Selective COX-2 inhibitor → ↓ GI side effects compared to non-selective NSAIDs; similar efficacy for dysmenorrhea ^[10]

Practical prescribing tips:

Start NSAIDs at onset of menses (or 1–2 days before if cycle is predictable) — prostaglandin production peaks in the first 48h of menstruation, so early dosing prevents the prostaglandin cascade from ramping up
Continue for 2–3 days (duration of pain)
Take with food to ↓ GI irritation
If one NSAID doesn't work, try a different one — there is inter-individual variation in response (possibly due to varying contributions of leukotrienes vs. prostaglandins)
If no improvement after trying 2–3 different NSAIDs over 3 menstrual cycles each, consider hormonal therapy

Contraindications to NSAIDs:

Contraindication	Why
Active peptic ulcer disease / GI bleeding	NSAIDs inhibit COX-1 → ↓ protective prostaglandins in gastric mucosa (PGE2 maintains mucosal blood flow, stimulates mucus/bicarbonate secretion) → ↑ risk of ulceration and bleeding
Renal impairment	Prostaglandins (via COX-1) maintain afferent arteriolar vasodilation in the kidney → NSAIDs → afferent vasoconstriction → ↓ GFR → can precipitate AKI, especially in those with pre-existing renal disease or dehydration
Severe asthma (aspirin-exacerbated respiratory disease)	COX inhibition shunts arachidonic acid metabolism towards the lipoxygenase pathway → ↑ leukotriene production → bronchospasm
Coagulopathy / anticoagulant therapy	NSAIDs ↓ thromboxane A2 (via COX-1 in platelets) → ↓ platelet aggregation → ↑ bleeding risk
Third trimester of pregnancy	Prostaglandins maintain patency of the ductus arteriosus; NSAIDs → premature closure → fetal pulmonary hypertension
Cardiovascular disease (for COX-2 selective)	COX-2 selective inhibitors ↓ endothelial prostacyclin (PGI2, which is vasodilatory and anti-thrombotic) without affecting platelet thromboxane → ↑ relative prothrombotic state → ↑ cardiovascular events

Why Mefenamic Acid Is Particularly Good for Dysmenorrhea

Mefenamic acid belongs to the fenamate class. Unlike other NSAIDs which only inhibit prostaglandin synthesis (via COX), fenamates also antagonise prostaglandin receptors directly. This dual action means they block both the production AND the action of prostaglandins. This is why mefenamic acid is often considered the NSAID of choice for dysmenorrhea specifically, though head-to-head trials show similar efficacy to ibuprofen and naproxen.

Step 3: Hormonal Therapy

Hormonal therapy is indicated as second-line when NSAIDs are insufficient, contraindicated, or when the patient also desires contraception. The fundamental principle is: suppress ovulation and/or reduce endometrial proliferation → ↓ prostaglandin production → ↓ pain.

These are particularly useful when oestrogen is contraindicated (e.g., smokers > 35, migraine with aura, history of VTE).

Method	Mechanism	Notes
Levonorgestrel-releasing intrauterine system (LNG-IUS / Mirena)	Releases levonorgestrel locally → endometrial atrophy (thin, inactive endometrium) → much less tissue to shed → ↓ prostaglandin production → ↓ pain. Also ↑ cervical mucus viscosity (contraceptive effect). Does NOT reliably suppress ovulation at standard dose.	Highly effective for dysmenorrhea AND menorrhagia. First-line for secondary dysmenorrhea associated with adenomyosis and heavy bleeding. Duration: 5 years. Common initial side effect: irregular spotting for 3–6 months (as endometrium adjusts)
Oral progestogen-only pill (POP)	Continuous progestogen → endometrial atrophy ± ovulation suppression (depends on type — desogestrel POP suppresses ovulation in ~97%)	Less effective than LNG-IUS for dysmenorrhea. Options: desogestrel 75 μg daily (continuous), norethisterone
Depot medroxyprogesterone acetate (DMPA / Depo-Provera)	IM injection every 12 weeks → high systemic progestogen → suppresses ovulation AND causes endometrial atrophy → amenorrhoea in many women → no menses = no dysmenorrhea	Very effective. Side effects: weight gain, irregular bleeding initially, delayed return of fertility (up to 12 months), ↓ BMD with prolonged use (usually reversible)
Subdermal implant (etonogestrel / Implanon)	Continuous progestogen release → suppresses ovulation in most cycles + endometrial atrophy	Duration: 3 years. Irregular bleeding is common. Effective for dysmenorrhea

Agent	Mechanism	Use in Dysmenorrhea
Danazol	Synthetic androgen derivative → suppresses HPO axis + direct inhibition of endometrial growth	Historically used for endometriosis. Now largely replaced by GnRH agonists due to significant androgenic side effects (hirsutism, acne, voice deepening, weight gain, hepatotoxicity)
Dienogest	Progestogen with specific anti-endometriotic activity → ↓ endometrial implant growth, ↓ angiogenesis, ↓ inflammation	Approved for endometriosis treatment. Dose: 2 mg daily. Fewer androgenic side effects than danazol
Aromatase inhibitors (letrozole, anastrozole)	Block aromatase enzyme → ↓ peripheral oestrogen production (adipose tissue, endometriotic implants themselves produce oestrogen via aromatase)	Used in refractory endometriosis (off-label). Must be combined with progestogen or GnRH agonist to prevent ovarian hyperstimulation (↓ oestrogen → ↓ negative feedback → ↑ FSH)

Procedure	Indication	Description
Laparoscopic excision / ablation of endometriosis	Confirmed endometriosis unresponsive to medical therapy; subfertility	Direct removal or thermal/laser destruction of endometriotic implants + adhesiolysis. Excision is preferred over ablation for deep infiltrating disease. Also allows staging (rASRM I–IV)
Presacral neurectomy (PSN)	Refractory midline pelvic pain (works best for midline pain; less effective for lateral pain)	Surgical interruption of the superior hypogastric plexus (presacral nerve) → interrupts afferent pain pathways from the uterus (T10–L1). Usually done laparoscopically as adjunct to endometriosis surgery. Risk: constipation, urinary dysfunction
Laparoscopic uterosacral nerve ablation (LUNA)	Previously used for chronic pelvic pain / dysmenorrhea	Ablation of the uterosacral ligaments at their uterine insertion → disrupts afferent nerve fibres. No longer recommended — RCTs show no benefit over diagnostic laparoscopy alone
Myomectomy	Fibroids causing symptoms (menorrhagia, dysmenorrhea, pressure symptoms) in women wishing to preserve fertility ^[1]	Removal of fibroids while preserving the uterus. Approach depends on fibroid location: hysteroscopic (submucous), laparoscopic or open (intramural/subserosal). Fibroids have a pseudo-capsule ^[1] → can be "shelled out" (enucleated) along this plane
Uterine artery embolisation (UAE)	Alternative to myomectomy/hysterectomy for symptomatic fibroids; not first-line if fertility desired	Interventional radiology: particles injected into uterine arteries → ischaemia of fibroids → shrinkage. Uterine tissue is more resistant to ischaemia than fibroid tissue due to collateral supply. Side effects: post-embolisation syndrome (pain, fever), potential effect on fertility (controversial)
Hysterectomy	Definitive treatment for refractory dysmenorrhea when fertility is no longer desired — especially for adenomyosis (adenomyosis cannot be enucleated like fibroids ^[1] because there is no pseudo-capsule), large/multiple fibroids, or failed medical therapy	Total hysterectomy (with or without bilateral salpingo-oophorectomy). For adenomyosis, hysterectomy is the only definitive cure because the disease is diffusely infiltrative. For endometriosis, hysterectomy alone is not curative (ectopic implants remain) — BSO may be added to remove oestrogen source, but this induces surgical menopause

Adenomyosis vs. Fibroids — Why Surgery Differs

Fibroids have a pseudo-capsule surrounding them ^[1] — this is compressed normal myometrium at the periphery of the tumour that creates a clear surgical plane. The surgeon can identify this plane and "shell out" (enucleate) the fibroid, preserving the uterus. Adenomyosis does not have a pseudo-capsule ^[1] — the ectopic endometrial glands are diffusely infiltrative within the myometrium with no clear boundary. You cannot simply cut it out without removing the entire uterus. This is why hysterectomy is the definitive treatment for adenomyosis, while myomectomy is the fertility-preserving option for fibroids.

B. Management of Secondary Dysmenorrhea — Cause-Specific

Approach	Options	Notes
Medical — first-line	NSAIDs (symptom control) + hormonal suppression: COCP (continuous preferred), progestogens (LNG-IUS, dienogest, DMPA), GnRH agonists (with add-back for > 6 months)	Goal: suppress oestrogenic stimulation of ectopic endometrial tissue → atrophy → ↓ pain. No single agent is superior; choice depends on side-effect profile, fertility desire, and patient preference
Surgical	Laparoscopic excision/ablation of implants + adhesiolysis ± cystectomy for endometriomas	Indicated when medical therapy fails or subfertility is the primary concern. Excision superior to ablation for deep disease. Recurrence rate ~40% at 5 years after surgery
Combined	Post-operative hormonal therapy to ↓ recurrence	COCP or progestogens after surgery significantly ↓ pain recurrence and endometrioma recurrence
Definitive	TAH + BSO + excision of all visible disease	For severe, refractory cases when fertility is complete. BSO removes the main oestrogen source. Must counsel about surgical menopause → may need HRT

Approach	Options	Notes
Medical — first-line	LNG-IUS (Mirena) — highly effective for both dysmenorrhea and menorrhagia in adenomyosis; causes local endometrial (and ectopic endometrial) atrophy. COCP, progestogens, GnRH agonists also used	LNG-IUS is preferred because local progestogen delivery directly suppresses ectopic endometrial glands within the myometrium
Surgical — definitive	Hysterectomy	Only cure — because adenomyosis is diffuse with no capsule. Fertility-sparing options (adenomyomectomy) exist but are technically challenging with high recurrence

Management will depend on the age, symptom, condition and wish of the patient ^[2].

Approach	Options	Notes
Expectant	Observation with serial USS	Appropriate for asymptomatic fibroids ^[1] — most fibroids are asymptomatic and do not require treatment. Fibroids shrink after menopause (loss of oestrogen drive)
Medical	LNG-IUS (↓ menorrhagia/dysmenorrhea); tranexamic acid (↓ menstrual blood loss — but contraindicated with COCP ^[11]); GnRH agonists (pre-operative shrinkage); GnRH antagonists (relugolix combination); iron supplementation for anaemia related to menorrhagia ^[1]	Medical therapy does not eliminate fibroids; it manages symptoms. GnRH agonists used for 3–6 months pre-operatively to shrink fibroids and correct anaemia before surgery
Surgical — fertility-preserving	Myomectomy (hysteroscopic for submucous; laparoscopic/open for intramural/subserosal)	Enucleation along the pseudo-capsule plane. Risk of recurrence (~15–30% require further surgery). Risk of uterine rupture in subsequent pregnancy if deep myometrial entry
Surgical — definitive	Hysterectomy	When fertility is complete and symptoms are severe/refractory
Interventional	UAE, MRI-guided focused ultrasound (MRgFUS)	Minimally invasive alternatives. UAE effective for symptom control but may affect fertility

Approach	Options	Notes
Antibiotics	Empirical broad-spectrum: ceftriaxone 500 mg IM stat + doxycycline 100 mg BD × 14 days + metronidazole 400 mg BD × 14 days	Must cover Chlamydia, Gonorrhoea, and anaerobes. Contact tracing and partner treatment essential
Drainage	USS-guided aspiration or surgical drainage	For tubo-ovarian abscess
Long-term	STI screening, contraception counselling, fertility assessment if future pregnancy desired	Tubal damage from PID → subfertility, ectopic pregnancy risk

Agent	Mechanism	Evidence / Notes
Paracetamol (acetaminophen)	Central COX inhibition and modulation of descending serotonergic pathways → ↑ pain threshold. Does NOT significantly inhibit peripheral prostaglandin production → less effective than NSAIDs for dysmenorrhea	Can be used as adjunct or in those who cannot tolerate NSAIDs. Less effective than NSAIDs as monotherapy for dysmenorrhea
Antispasmodics (hyoscine butylbromide / Buscopan)	Antimuscarinic → ↓ smooth muscle spasm (including myometrium)	Some evidence of benefit as adjunct; not first-line
Vitamin B1 (thiamine), Vitamin E, Magnesium	Various proposed mechanisms: Mg → smooth muscle relaxation; Vitamin B1 → modulation of prostaglandin synthesis; Vitamin E → antioxidant, ↓ prostaglandin production	Limited but positive evidence from small RCTs; can be suggested as supplements
Psychological therapies (CBT, mindfulness)	Modulate central pain processing, ↓ catastrophising, ↓ anxiety	Important adjunct, especially in chronic pelvic pain and when pain persists despite adequate treatment of identifiable causes

Line	Primary Dysmenorrhea	Secondary Dysmenorrhea
First-line	Non-pharmacological measures + NSAIDs	Treat underlying cause + NSAIDs for symptom control
Second-line	Hormonal therapy (COCP, progestogens)	Hormonal suppression (LNG-IUS, COCP, GnRH agonists — cause-dependent)
Third-line	Investigate for secondary cause; consider laparoscopy	Surgical intervention (laparoscopic excision for endometriosis, myomectomy for fibroids)
Definitive	Rarely needed for primary	Hysterectomy ± BSO (when fertility complete and medical/conservative surgery fails)

Failure of first- and second-line therapy after adequate trial (3–6 months)
Suspected secondary cause requiring further investigation (pelvic mass, subfertility, abnormal examination)
Desire for surgical management
Adolescent with severe dysmenorrhea from menarche non-responsive to treatment → suspect structural anomaly

High Yield Summary

First-line for primary dysmenorrhea: NSAIDs (ibuprofen, naproxen, or mefenamic acid). Start at onset of menses. Effective in ~80%. Mefenamic acid has dual action (COX inhibition + prostaglandin receptor blockade).

Second-line: Hormonal therapy — COCP (suppresses ovulation → thin endometrium → ↓ prostaglandins) ^[11]. Contraindications include uncontrolled CV risk factors, active smoking, and concomitant tranexamic acid use ^[11]^[12].

LNG-IUS (Mirena): Highly effective for both primary and secondary dysmenorrhea (especially adenomyosis), provides contraception, causes local endometrial atrophy.

GnRH agonists: Create "medical menopause" — reserved for severe endometriosis/adenomyosis. Limited to 6 months without add-back therapy due to bone loss.

Surgical key points: Fibroids can be enucleated (myomectomy) because they have a pseudo-capsule. Adenomyosis cannot be enucleated because it has no pseudo-capsule ^[1] → hysterectomy is the only definitive cure.

Non-response to NSAIDs + COCP after 3–6 months → reconsider diagnosis, investigate for secondary causes.

Management depends on age, symptoms, condition, and wish of the patient ^[2].

Active Recall - Management of Dysmenorrhea

References

^[1] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[2] Lecture slides: GC 118. Pelvic mass ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[10] Senior notes: Ryan Ho Rheumatology.pdf (Section on NSAIDs/COX-2 inhibitors in spondyloarthritis — principles of NSAID use) ^[11] Lecture slides: Block C - O&G Theme Case 2.docx.pdf (COC pills, contraindications including concomitant tranexamic acid) ^[12] Lecture slides: Block C - Climacteric symptoms_ menopause and related illness; amenorrhoea.pdf (HRT contraindications — severe liver disease, cerebrovascular disease, DVT/embolism, oestrogen-dependent tumours, undiagnosed uterine bleeding) ^[13] Senior notes: Ryan Ho Endocrine.pdf (Section 2.4 — Osteoporosis, oestrogen and bone remodelling, RANKL/OPG system)

Complications of Dysmenorrhea

Complications of dysmenorrhea can be divided into those arising from primary dysmenorrhea itself (which are mostly functional and quality-of-life related, rather than structural) and those arising from the underlying causes of secondary dysmenorrhea (which can be severe and irreversible). It is important to understand that primary dysmenorrhea, while not "dangerous" in the traditional sense, carries a significant burden of morbidity. Secondary causes, if undiagnosed or untreated, carry the risk of serious long-term sequelae.

A. Complications of Primary Dysmenorrhea

Primary dysmenorrhea does not cause structural pelvic damage (by definition, there is no pelvic pathology). However, its complications are real and clinically significant:

Because women with primary dysmenorrhea use NSAIDs and hormonal therapies cyclically over many years, they are at risk of treatment-related adverse effects:

Complication	Mechanism	Notes
NSAID gastropathy (dyspepsia, peptic ulcer, GI bleeding)	COX-1 inhibition → ↓ protective gastric prostaglandins (PGE2 maintains mucosal blood flow, mucus and bicarbonate secretion) → mucosal vulnerability → erosion/ulceration	Risk is cumulative with long-term use. Mitigated by taking NSAIDs with food, using the lowest effective dose, co-prescribing PPI if high-risk
NSAID-related renal effects	COX-1/2 inhibition → ↓ prostaglandin-mediated afferent arteriolar vasodilation → ↓ GFR. Usually only clinically significant if pre-existing renal impairment, dehydration, or concomitant nephrotoxic drugs	Rare in young healthy women using intermittent short courses
Hormonal therapy side effects	COCP: VTE risk (oestrogen ↑ hepatic synthesis of clotting factors), headaches, mood changes, breast tenderness. Progestogens: irregular bleeding, weight gain, mood changes. GnRH agonists: bone density loss, menopausal symptoms	Appropriate patient selection and counselling are essential
Medication overuse / analgesic dependence	Frequent use of combination analgesics (especially those containing codeine/caffeine) → habituation → need for escalating doses; can develop medication overuse headache if headache is a prominent associated symptom	Codeine-containing analgesics should generally be avoided for dysmenorrhea

B. Complications of Secondary Dysmenorrhea (Cause-Specific)

These are the complications of the underlying conditions. They are the real danger — and the reason we must always consider secondary causes.

Complication	Mechanism	Clinical Impact
Subfertility	Multiple mechanisms: (1) Adhesions distort tubo-ovarian anatomy → impair oocyte pickup; (2) Peritoneal inflammation creates hostile environment for sperm/embryo; (3) Endometriomas destroy ovarian reserve; (4) Endometrial receptivity may be impaired	Affects ~30–50% of women with endometriosis. One of the most common causes of female subfertility
Adhesion formation	Chronic peritoneal inflammation → fibrin deposition → fibroblast proliferation → dense fibrous adhesions that tether pelvic organs (uterus, tubes, ovaries, bowel, bladder)	Causes chronic pelvic pain (organs are pulled during movement), dyspareunia, bowel/bladder dysfunction, and contributes to subfertility
Endometrioma rupture	Endometrioma ("chocolate cyst") on ovary → wall ruptures → spills old blood and inflammatory contents into peritoneal cavity → chemical peritonitis	Acute abdomen, severe pain, may require emergency surgery. Especially painful if dermoid cyst rupture ^[6]
Deep infiltrating endometriosis	Endometriotic implants invade deeply ( > 5 mm) into pelvic structures — rectovaginal septum, uterosacral ligaments, bladder wall, bowel wall	Dyschezia, dysuria during menses, bowel obstruction (rare), ureteric obstruction → hydronephrosis (rare)
Malignant transformation	Rare (< 1%) but well-documented: endometriosis (particularly endometriomas) can undergo malignant transformation → endometrioid or clear cell ovarian carcinoma	Long-term surveillance of endometriomas is recommended; risk increases with age and prolonged disease duration

Complication	Mechanism	Clinical Impact
Chronic menorrhagia → iron deficiency anaemia	Enlarged uterus with ectopic endometrial glands → ↑ endometrial surface area + disrupted myometrial contractility → inability to compress spiral arteries effectively → heavy, prolonged bleeding	Anaemia related to menorrhagia ^[1] — fatigue, pallor, exertional dyspnoea. May be severe enough to require iron infusion or transfusion
Subfertility	Disrupted junctional zone → impaired uterine peristalsis (which normally facilitates sperm transport) + altered endometrial receptivity → impaired implantation	Increasingly recognised as a cause of subfertility and recurrent implantation failure in IVF
Pregnancy complications	Adenomyotic uterus has abnormal myometrial architecture → ↑ risk of miscarriage, preterm labour, abnormal placentation (placenta praevia, placenta accreta spectrum), and PPH (impaired contraction of abnormal myometrium)	Important to recognise in women undergoing fertility treatment

Fibroids classically do NOT cause dysmenorrhea ^[1] — a pure fibroid will seldom cause dysmenorrhea, so have to think of adenomyosis ^[1]. However, there are two exceptions ^[1]:

Heavy bleeding related to the fibroid will cause clot formation in the uterus, and uterus will try to expel these clots, causing pain ^[1]
Pedunculated fibroid in the uterine cavity — uterus will think foreign body and want to expel → hence dysmenorrhea sensation ^[1]

Complication	Mechanism	Clinical Impact
Menorrhagia → iron deficiency anaemia	↑ surface area of overlying endometrium → ↑ bleeding ^[14]; submucosal fibroids distort the cavity; may also cause surface ulceration/necrosis → irregular heavy bleeding	Anaemic symptoms in prolonged heavy bleeding ^[14]. May require iron supplementation, transfusion, or surgical intervention
Pressure symptoms ^[14]	Irregularly enlarged uterus compresses adjacent structures	Urinary frequency (anterior fibroid compresses bladder), rarely AROU (acute retention of urine — classically a 12-week uterus with cervical fibroid or posterior fibroid pushing on retroverted uterus → kinking of urethra) ^[14], hydronephrosis (lateral fibroid compresses ureter), tenesmus (posterior fibroid compresses bowel) ^[14], venous compression (very large uteri → compress vena cava → ↑ risk of VTE) ^[14]
Red degeneration ^[14]	Classically occur in mid-2nd trimester of pregnancy ^[14] — rapid fibroid growth outstrips blood supply → haemorrhagic infarction of the fibroid	Acute pain, localised tenderness, low-grade fever, ↑ WCC. Usually managed conservatively with analgesia and rest
Torsion of pedunculated fibroid ^[14]	Pedunculated subserosal fibroid twists on its stalk → venous congestion → oedema → arterial compromise → ischaemic necrosis	Acute pain ± fever ^[14]. May require emergency surgery
Fibroid polyp prolapse ^[14]	Submucous pedunculated fibroid descends through the cervical os → uterine contractions attempt to expel it → profuse bleeding if fibroid polyp protrudes through cervix ^[14]	Pain, heavy bleeding, risk of infection. Requires hysteroscopic removal
Pregnancy-related complications ^[14]	Infertility (controversial but appears ↑ in those with cavity distortion), miscarriage and preterm labour (submucosal fibroids impair implantation, increase contractility), malpresentation and obstructed labour (distortion of birth canal), Caesarean section difficulty (lower segment fibroids), PPH (↓ force and coordination of uterine contractions → ↑ risk of atony) ^[14]	Important to assess fibroid location and size in pregnancy planning
Sarcomatous transformation	Extremely rare (< 0.5%) — leiomyosarcoma may arise de novo in the myometrium rather than true transformation of a fibroid. However, rapidly growing fibroid (especially post-menopause when fibroids should be shrinking) raises concern	Rapidly enlarging "fibroid" in a postmenopausal woman → suspect leiomyosarcoma → urgent MRI + surgical evaluation

Complication	Mechanism	Clinical Impact
Tubo-ovarian abscess ^[14]	Severe ascending infection → walled-off collection of pus involving the tube and ovary	75% will respond to antibiotics alone; surgical drainage if ≥ 7 cm, not responding to IV antibiotics in 48–72h, or signs of rupture ^[14]
Chronic pelvic pain (15–20%) ^[14]	Result from scarring and adhesions from PID-associated inflammation ^[14] — definition: menstrual or non-menstrual pain for ≥ 6 months occurring below umbilicus → dysmenorrhea, dyspareunia ^[14]	Significant quality-of-life impact. May require multidisciplinary pain management
Ectopic pregnancy (7× ↑ risk) ^[14]	Due to tubal blockage ^[14] — PID damages tubal epithelium (loss of ciliary action, fibrosis, partial occlusion) → fertilised ovum cannot transit to uterus → implants in tube	Life-threatening if ruptured. Must always rule out in woman with PID history presenting with pain + positive pregnancy test
Subfertility (~20%) ^[14]	13% after 1 episode, 36% after 2 episodes, 75% after 3 episodes ^[14]. Reason: loss of ciliary action, fibrosis, tubal occlusion ^[14]	Dose-dependent relationship with number of PID episodes. Prevention of recurrence is critical
Recurrent PID (25%) ^[14]	Incomplete eradication, reinfection from untreated partners, persistent risk behaviour	Risk factors for recurrence: chlamydia infection, delay in seeking care (≥ 3 days), ↑ PID episodes, ↑ PID severity ^[14]
Fitz-Hugh-Curtis syndrome ^[14]	Perihepatitis — infection spreads from the pelvis to the liver capsule (either by direct spread along peritoneum or via lymphatics/haematogenous) → "violin string" adhesions between liver capsule and anterior abdominal wall	Right upper quadrant pain that may mimic biliary disease, pleurisy, or pulmonary embolism. Important differential in young women with RUQ pain

Complication	Mechanism	Presentation
Rupture	Cyst wall breaks (spontaneously, during activity, or during intercourse) → cyst contents spill into peritoneal cavity → chemical peritonitis (especially painful with dermoid cyst contents — hair, sebum, tooth — causing intense foreign body reaction)	Sudden onset lower abdominal pain, often with strenuous physical activity ^[6]; may cause haemoperitoneum if vascular → haemodynamic instability
Torsion	Cyst adds mass to the ovary → ovary twists on its vascular pedicle (infundibulopelvic ligament) → venous obstruction → congestion → oedema → arterial compromise → ischaemic necrosis	Often a/w waves of nausea and vomiting ± fever/↑WCC (suggests necrosis) ^[6]. Surgical emergency — requires urgent detorsion ± oophorectomy
Haemorrhage	Bleeding into the cyst (corpus luteum cyst is particularly prone) → rapid enlargement → pain; may rupture secondarily	Acute unilateral pain; USS shows complex cyst with internal echoes

Treatment	Complication	Mechanism
NSAIDs (long-term cyclical use)	GI bleeding, peptic ulceration, renal impairment, cardiovascular events (COX-2 selective)	As discussed in management section
COCP	VTE, stroke (especially migraine with aura), hepatic adenoma (rare, long-term use)	Oestrogen ↑ hepatic clotting factor synthesis → prothrombotic state
GnRH agonists	Bone mineral density loss, menopausal symptoms, mood disturbance	Hypo-oestrogenic state → ↑ RANKL → osteoclast activation → bone resorption ^[13]
Myomectomy	Uterine rupture in subsequent pregnancy, adhesion formation, fibroid recurrence (15–30%)	Deep myometrial entry weakens the uterine wall; raw surfaces form adhesions
Hysterectomy	Surgical menopause (if BSO performed), urinary tract injury, wound infection, VTE, psychological impact	Removal of ovaries → abrupt oestrogen withdrawal → menopausal symptoms; anatomical proximity of ureters to uterine arteries → risk of ureteric injury

High Yield Summary

Primary dysmenorrhea complications are mainly functional (absenteeism, psychological impact, medication side effects) but can lead to central sensitisation → chronic pelvic pain syndrome if undertreated.

Delayed diagnosis is the most dangerous "complication" of primary dysmenorrhea — failure to recognise secondary causes (especially endometriosis) leads to progressive disease and irreversible subfertility.

Endometriosis complications: subfertility (30–50%), adhesions, endometrioma rupture, deep infiltrating disease (bowel/bladder/ureteric involvement), rare malignant transformation.

Fibroid complications: menorrhagia → anaemia, pressure symptoms (urinary frequency, AROU, hydronephrosis, tenesmus, VTE), red degeneration (pregnancy), torsion, fibroid polyp prolapse, pregnancy complications (miscarriage, malpresentation, PPH) ^[14]. Fibroids classically do NOT cause dysmenorrhea except: (1) heavy bleeding with clot expulsion, (2) pedunculated fibroid acting as foreign body ^[1].

PID complications: TOA, chronic pelvic pain (15–20%), ectopic pregnancy (7× ↑), subfertility (13% after 1 episode, 36% after 2, 75% after 3), recurrent PID (25%), Fitz-Hugh-Curtis ^[14].

Central sensitisation: repeated intense pain → dorsal horn hyperexcitability → pain persists between menses → chronic pelvic pain syndrome. Early adequate treatment may prevent this.

Active Recall - Complications of Dysmenorrhea

References

^[1] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf ^[6] Senior notes: Ryan Ho GI.pdf (Differential diagnoses in adult females — ovarian cyst complications) ^[13] Senior notes: Ryan Ho Endocrine.pdf (Section 2.4 — Osteoporosis, oestrogen and bone remodelling, RANKL/OPG system) ^[14] Senior notes: Adrian Lui Gynecology Notes.pdf (Sections 2.3 — Dysmenorrhea; fibroid complications; PID complications; UAE complications)

High Yield Summary

Definition: Painful menstruation — crampy suprapubic/pelvic pain temporally related to menses.

Classification:

Primary: Pain without identifiable pelvic pathology (diagnosis of exclusion).
Secondary: Underlying pathology (most commonly endometriosis).

Epidemiology: 45–95% of menstruating women; 10–20% severe; leading cause of school/work absenteeism in young women.

Primary dysmenorrhoea pathophysiology:

Progesterone withdrawal → phospholipase A2 → arachidonic acid → COX → PGF2α + PGE2.
PGF2α → myometrial hypercontractility + spiral artery vasoconstriction → uterine ischaemia ("uterine angina").
Only in ovulatory cycles — explains onset 1–2 years post-menarche.
Women with primary dysmenorrhoea have 2–7× higher endometrial prostaglandins.

Primary features: Crampy pain with/onset of menses, lasts 48–72 h; nausea, vomiting, diarrhoea, headache (systemic PGs); normal pelvic exam; responds to NSAIDs/COCP (~80%).

Secondary red flags: Onset >25 years or new/progressive; pain before/after menses; menorrhagia; dyspareunia, dyschezia; subfertility; abnormal exam; failure of NSAIDs/COCP.

Top secondary causes (HK): (1) Endometriosis, (2) Adenomyosis, (3) Fibroids, (4) Cu-IUD, (5) PID.

Primary vs secondary exam:

Primary: normal-sized, non-tender uterus.
Adenomyosis: uniformly enlarged, boggy, tender.
Endometriosis: POD nodularity, fixed retroverted uterus.
Fibroids: irregular, firm, discrete lumps.

High Yield Summary — Differential Diagnosis

Organise by system:

Gynaecological — uterine:

Primary dysmenorrhoea, adenomyosis, fibroids, cervical stenosis, uterine anomalies, Cu-IUD.

Gynaecological — adnexal/peritoneal:

Endometriosis (most common secondary), ovarian cyst complications, mittelschmerz, ectopic pregnancy.

Gynaecological — infectious: PID (discharge, fever, cervical excitation).

Non-gynaecological:

IBS (worsens with menses; not purely cyclical — huge overlap with endometriosis).
IBD, appendicitis (acute).
Interstitial cystitis, UTI, ureteric colic.
Myofascial pelvic pain, somatoform disorder.

Emergencies (acute pelvic pain): Ruptured ectopic, ovarian torsion, ruptured cyst, appendicitis, TOA — always β-hCG.

Feature	Primary	Endometriosis	Adenomyosis	Fibroids
Onset	Teens	25–35	35–50	30–50
Pain timing	With menses only	Pre/post-menses	Menstrual	Variable
Dyspareunia	No	Deep	No	No
Exam	Normal	POD nodularity	Boggy uterus	Firm lumps

Failure of NSAIDs + COCP after 3–6 months → investigate secondary cause (USS ± laparoscopy).

High Yield Summary — Diagnosis

Primary dysmenorrhoea — clinical diagnosis of exclusion (all required):

Cyclical suprapubic pain with menses (≤72 h).
Onset 1–2 years post-menarche.
No red flags.
Normal pelvic examination.
Response to NSAIDs/COCP.

Adolescent not sexually active: May trial empirical Rx without exam if classic + no red flags; examine if non-responsive.

Mandatory first test: β-hCG in any reproductive-age woman.

When to investigate secondary:

Red flags, sexually active, age >25, non-response to 3–6 months empirical Rx.

Investigation strategy:

Scenario	Workup
Classic primary (adolescent)	None if responds to Rx
Suspected secondary	Pelvic USS (TVS) ± MRI
Suspected endometriosis	USS → MRI → diagnostic laparoscopy if refractory
Menorrhagia + dysmenorrhoea	USS — adenomyosis vs fibroids
Severe from menarche, non-responsive	3D USS/MRI for Müllerian anomaly

USS distinctions:

Fibroids: Well-circumscribed, pseudocapsule, hypoechoic whorled.
Adenomyosis: Diffuse heterogeneous myometrium, cysts, no pseudocapsule.
Endometrioma: Ground-glass ovarian cyst.

CA125: Not for endometriosis screening; useful only with ovarian mass (RMI).

Hormonal workup (FSH, PRL, TFT): Only if coexisting amenorrhoea/oligomenorrhoea.

High Yield Summary — Management

Primary dysmenorrhoea — stepwise:

Step	Treatment	Notes
1	Lifestyle: exercise, heat, diet (omega-3)	Heat ≈ ibuprofen in RCTs
2	NSAIDs first-line	Start at/onset of menses; mefenamic acid blocks PG synthesis + receptors; ~80% respond
3	COCP (continuous preferred)	Suppresses ovulation → ↓ PG production; ~90% effective
4	Progestins (Mirena, DMPA)	If COCP CI
5	Reconsider secondary; USS ± laparoscopy	After 3–6 months failure

NSAIDs CI: PUD, renal impairment, aspirin-exacerbated asthma, anticoagulation, 3rd trimester.

COCP CI: VTE, migraine with aura, smoking >35, concomitant tranexamic acid (both prothrombotic).

Secondary — treat underlying cause:

Cause	Management
Endometriosis	NSAIDs + COCP/progestins → GnRH agonist → lap excision; fertility pathway separate
Adenomyosis	Mirena, COCP, GnRH agonist → hysterectomy
Fibroids	Mirena, GnRH agonist pre-op → myomectomy or hysterectomy
PID	Antibiotics + partner treatment
Cu-IUD	Switch to Mirena or remove

Surgical pearls:

Fibroids: Myomectomy (pseudocapsule — can enucleate).
Adenomyosis: Hysterectomy only (no capsule).
Endometriosis: Lap excision/ablation ± post-op Mirena.

Referral: Non-response, suspected secondary, adolescent severe from menarche, desire for surgery.

High Yield Summary — Complications

Primary dysmenorrhoea (functional, not structural):

Absenteeism — most common gynaecological cause of school/work loss.
Central sensitisation → chronic pelvic pain syndrome if undertreated.
Psychological: anxiety, depression, anticipatory pain.
Medication-related: NSAID gastropathy, COCP VTE; medication overuse headache.
Delayed secondary diagnosis — most dangerous "complication" (missed endometriosis 7–10 years).

Secondary cause complications:

Endometriosis: Subfertility (25%), adhesions, endometrioma rupture, DIE (bowel/ureter/bladder), malignant transformation (< 1%), central sensitisation.

Adenomyosis: Anaemia, subfertility, adverse pregnancy outcomes, chronic pain.

Fibroids — classically NOT dysmenorrhoea except:

Heavy bleeding → clot expulsion pain.
Pedunculated submucous → "foreign body" expulsion pain. Complications: menorrhagia → anaemia, pressure symptoms, red degeneration (pregnancy), torsion, PPH.

PID: TOA; subfertility 13%/36%/75% after 1/2/3 episodes; ectopic 7×; chronic pelvic pain 15–20%; Fitz-Hugh-Curtis.

Treatment-related: GnRH agonist bone loss; myomectomy → uterine rupture in pregnancy; hysterectomy surgical risks.

Dysmenorrhea

Definition

Epidemiology

Anatomy and Function

Uterine Anatomy

The Normal Menstrual Cycle (Relevant to Dysmenorrhea)

Etiology and Pathophysiology

A. Primary Dysmenorrhea

B. Secondary Dysmenorrhea

Classification

By Etiology (Most Clinically Used)

By Severity (Andersch & Milsom Grading, sometimes used in research)

Clinical Features

A. Primary Dysmenorrhea

Symptoms

Signs

B. Secondary Dysmenorrhea

"Red Flags" Suggesting Secondary Dysmenorrhea

Cause-Specific Clinical Features

Summary of Key Differentiating Features: Primary vs. Secondary Dysmenorrhea

Active Recall - Dysmenorrhea (Definition to Clinical Features)

References

Organising Framework for the Differential Diagnosis

A. Gynaecological Causes

1. Primary Dysmenorrhea (Diagnosis of Exclusion)

2. Endometriosis

3. Adenomyosis

4. Uterine Fibroids (Leiomyomata)

5. Pelvic Inflammatory Disease (PID)

6. Ovarian Cysts and Masses

7. Endometrial Polyps

8. Cervical Stenosis

9. Uterine Anomalies (Müllerian Anomalies)

10. Intrauterine Device (Copper IUD)

11. Ectopic Pregnancy

12. Mittelschmerz ("Middle Pain")

B. Non-Gynaecological Causes

1. Gastrointestinal

2. Urological

3. Musculoskeletal

4. Psychogenic / Functional

C. Approach to Differentiating Primary vs. Secondary Dysmenorrhea and Narrowing the Differential

D. Summary Table: Complete Differential Diagnosis of Dysmenorrhea

Active Recall - Differential Diagnosis of Dysmenorrhea

Diagnostic Criteria

Primary Dysmenorrhea — A Clinical Diagnosis of Exclusion

Secondary Dysmenorrhea — Diagnosis Depends on the Underlying Cause

Diagnostic Algorithm

Investigation Modalities

1. Baseline Blood Tests

2. Hormonal Investigations

3. Pelvic Ultrasound (First-Line Imaging)

4. Advanced Imaging

5. Endoscopic / Surgical Investigation

6. Other Investigations

Putting It All Together: Investigation Strategy by Clinical Scenario

Active Recall - Diagnostic Criteria, Algorithm, and Investigations for Dysmenorrhea

Management Algorithm

A. Management of Primary Dysmenorrhea

Step 1: Non-Pharmacological Measures

Step 2: NSAIDs — First-Line Pharmacological Therapy

Step 3: Hormonal Therapy

A. Combined Oral Contraceptive Pill (COCP)

B. Progestogen-Only Methods

C. GnRH Agonists

D. GnRH Antagonists (Newer Agents)

E. Other Hormonal Options

Step 4: Surgical and Interventional Options (for Refractory Primary or Secondary Dysmenorrhea)

B. Management of Secondary Dysmenorrhea — Cause-Specific

1. Endometriosis

2. Adenomyosis

3. Uterine Fibroids

4. PID

5. Copper IUD

Adjunctive Therapies (Applicable to Both Primary and Secondary)

Summary Table: Management by Line of Therapy

Indications for Referral to Gynaecology

Active Recall - Management of Dysmenorrhea

A. Complications of Primary Dysmenorrhea

1. Functional Impairment and Reduced Quality of Life