dysmenorrhea ,dysmenorrhea definition, types of dysmenorrhea, menstrual pain , pathophysiology of dysmenorrhea, management of primary dysmenorrhea, management of secondary dysmenorrhea, treatment of dysmenorrhea.

1. DYSMENORRHEA
DEFINITION: dysmenorrhea is a cyclical pain associated with
menstruation – “painful menstruation”, that significantly interferes
with day to day pursuits. It is a common gynaecological disorder
affecting 60% of menstruating females.
TYPES:
 Primary dysmenorrhea
 Secondary dysmenorrhea
PRIMARY DYSMENORRHEA:
Primary dysmenorrhea is otherwise called as spasmodic
dysmenorrhea. It occurs in normal ovulatory cycle without any
conspicuous pelvic or uterine pathology.
INCIDENCE:
Incidence of primary dysmenorrhea is about 15 - 20%.
Prevails mainly in adolescent girls within 1 to 2 years of menarche
usually from opulent society, with high BMI and with familial
association. Parity (mainly after vaginal delivery) appears to improve
symptoms.
PATHOPHYSIOLOGY:
Mechanisms postulated in the pathophysiology of primary
dysmenorrhea are;
 Psychosomatic and lifestyle factors

2.  Effects of Prostaglandins
 Effects of autonomic nerves
 Effects of progestrone levels
 Effects of vasopressin
 Effects of Endothelins, Platelet Activating Factor
(PAF), and Leukotrienes
 Abnormal myometrial anatomy
Psychosomatic and lifestyle factors:
 Tension, anxiety and stress - lowers the pain threshold
 Long menstrual period
 Smoking, over weight and sedentary life style has its impact
on primary dysmenorrhea.
Effects of Prostaglandins:
• Effects of prostaglandins in pathophysiology of primary
dysmenorrhea is explained by, excessive or imbalanced
synthesis of PGE2 & PGF2α or due to increased sensitivity of
myometrium to normal prostaglandins during menstruation,
resulting in dysperistalsis and hyperactivity of myometrium and
vasoconstriction resulting in myometrial ischemia and pain.

3. Pathophysiology

4. Endometrial Breakdown in
Menses.
Excessive Or Imbalanced PGE2
& PGF2α
Dysperistalsis And
Hyperactivity.
1.Dysrhythmic Contraction,
2.Increased Basal Tone,
3.Increased Active Pressure,
4.Uterine Hypercontractility.
Strong Vasoconstriction Myometrial Ischemia
Pain.

5. Effects of autonomic nerves:
This pain can be relived by dilatation of cervix by
damaging sensory nerve endings of but later may lead to
incompetence. The same mechanism is explained for pain relief
following vaginal delivery.
Effects of progestrone levels:
The low levels of progesterone in the late luteal phase
triggers lytic enzymatic action, resulting in a release of phospholipids
with the generation of arachidonic acid and activation of the cyclo-
oxygenase (COX) pathway.
Pain.
Hypertonicity
of Circular
Fibers of
Isthumus and
Internal Os.
Hyperactivity
Of
Sympathetic
Nerves.

6. Thus prostaglandin, thromboxane and leukotrienes are
derived from arachidonic acid.
Effects of vasopressin:
Increased levels of vasopressin is noted in females with
primary dysmenorrhea. It acts directly on the myometrium and causes
hyperactivity, it also increases prostaglandins synthesis and in turn
results in uterine hyperactivity and dysrhythmic contraction leading to
•Declined
Progestrons
Triger lytic
Enzyme
•Generation of
arachidonic acid
•Release of
phospholipids
Activation of
COX pathway •prostaglandins
•thromboxane
•leukotrienes.
pain.

7. ischemia, hypoxia and pain.
Effects of Endothelins, Platelet Activating Factor (PAF), and
Leukotrienes:
Increased
Levels Of
Vasopressin
Myometrial
Hyperactivity
+
Increased PG
Uterine
Hyperactivity,
Dysrhythmic
Contraction.
Pain
Endothelins,
Platelet
Activating
Factor (PAF),
and
Leukotrienes
Increased
Myometrial
Contractions
In Jz, +/-
Dysrhythmia.
Pain

8. Abnormal myometrial anatomy:
Abnormality in junctional zone (JZ) – sub endometrial
layer of myometrium like hyperplasia, irregular thickening and less
vascularity resulting in dysperistalsis and hyperactivity of
myometrium causing pain.
CLINICAL FEATURES:
The hallmarks of primary dysmenorrhea are:
The pain of primary dysmenorrhea usually begins a few
hours before or just after the onset of a menstrual period and may last
48 to 72 hours.
The pain of dysmenorrhea is spasmodic / colicky in nature
and, is relieved by abdominal massage, counter-pressure, or
movement of the body. The pain is labour - like, with suprapubic
cramping, and may be accompanied by lumbosacral backache, pain
radiating down the anterior and inner thighs.
Accompanied by generalized weakness nausea, vomiting,
diarrhoea, vasomotor symptoms and rarely syncopal episodes.
Pelvic and bimanual examination does not reveal any
pathology.
MANAGEMENT:
Investigation:
Investigations are done to rule out any underlying pelvic
pathology.

9. NAAT or culture for gonorrhoea and chlamydia are done to
rule out PID.
Pelvic ultrasound should be done if symptoms do not resolve
with NSAIDs.
Diagnosis of primary dysmenorrhea is made after considering
symptoms and excluding pathologies.
If symptoms persist laparoscopy can also be performed.
Treatment:
General considerations like improving general health and hygiene,
frequent bladder and bowel emptying and encouraging to do day to
day activities and simple sport activities. Counselling and
reassurance, with NSAIDs will work for most of the females.
Medical management:
Treatment
Medical
Non
hormonal
Hormonal
Surgical
TENS
LUNA
LPSN
Cervical
dilatation.

10. Nonsteroidal anti-inflammatory agents, are effective for the
treatment of primary dysmenorrhea. NSAIDs - Prostaglandin synthase
inhibitors are effective in treatment of primary dysmenorrhea as there
is strong relation of increased PGs with primary dysmenorrhea.
NSAIDs should be taken up to 1 to 3 days before or, if menses
are irregular, at the first onset of even minimal pain or bleeding and
then continuously every 6 to 8 hours to prevent reformation of
prostaglandin by-products for 3 to 6 months.
Side effects - nausea, dyspepsia, diarrhoea, and occasionally
fatigue.
Contraindication - gastrointestinal ulcers or bronchospastic
hypersensitivity to aspirin.
Selective COX-2 inhibitors have similar analgesic effect but
with fewer side effects.
Commonly Used Oral Nonsteroidal Anti-inflammatory Drugs
(NSAIDs) in the Treatment of Dysmenorrhea
Generic Name Dosage
Ibuprofen 400 mg every 4–6 hr
Naproxen 500 mg initially, then 250 mg
every 6–8 hr
Naproxen
sodium
550 mg initially, then 275 mg
every 6–8 hr
Mefenamic
acid
500 mg initially, then 250 mg
every 6 hr
Ketoprofen 50 mg every 6–8 hr

11. COX-2 inhibitor:
Generic name Dosage
Celecoxib 200mg every 12hr
Hormonal contraceptives:
Hormonal contraceptives are considered for;
Patients who are unresponsive or have contraindications
to NSAIDs.
Patients who have no contraindications to hormonal
contraceptive and who desire contraception.
Combined oestrogen and progestin or progesterone only
oral contraceptives given continuous or as cyclic regime.
Transdermal patch, vaginal ring, injectable progestin
preparations, or levonorgestrel-releasing intrauterine devices
(LNG-IUS) are more effective than placebo alone.
Hormonal contraceptives inhibit ovulation, decrease
endometrial proliferation, and create an endocrine milieu similar
to the early proliferative phase of the menstrual cycle, when
prostaglandin levels are lowest. Decreased prostaglandin levels
result in less uterine cramping.

12. Hormonal contraceptives
GnRH agonists and androgens:
The oestrogen-lowering effects of these drugs lead to endometrial
atrophy and diminished prostaglandin production resulting in no or less pain.
Inhibits Ovulation
Decreased
endometrial
proliferation
Low PGs
Less / no pain.

13. Nonpharmacologic pain management:
Heat, acupuncture, or transcutaneous electrical nerve stimulation
(TENS), may be useful but not effective as medical management.
Surgical:
Laparoscopic procedures like LUNA , LPSN have limited
effects in primary dysmenorrhea.
LUNA – laparoscopic uterine nerve ablation.
LPSN – laparoscopic presacral neurectomy.
Dilatation of cervical canal helps in females with primary
dysmenorrhea with cervical stenosis by damaging the sensory nerve
endings, still it has its risk of cervical incompetence later.
SECONDARY DYSMENORRHEA:
Secondary dysmenorrhea is otherwise called as congestive
dysmenorrhea. Secondary dysmenorrhea is cyclic menstrual pain
that occurs in association with underlying pelvic pathology.
INCIDENCE: It is variable and depends on the type of pelvic
pathology. Usually seen in their thirties, more often parous and not
related to any SES.

14. PATHOPHYSIOLOGY:
In congestive or secondary dysmenorrhea the pain is due to
increased pelvic tissue tension caused by premenstrual pelvic
congestion or increased vascularity in pelvic organs.
CLINICAL FEATURES:
The pain of secondary dysmenorrhea often begins 1 to 2
weeks before menstrual flow and persists until a few days after the
cessation of bleeding.
Pain is dull aching and mostly confined to back and not
usually radiating / not associated with vasomotor symptoms.
Pelvic and bimanual examination reveals pelvic pathology.
secondary dysmenorrhea frequently complicates or
associated with endometriosis, leiomyomas, PID, adenomyosis,
endometrial polyps, and menstrual outlet obstruction - And hence, it
pelvic pathology
Increased vascularity
Premenstrual Pelvic
Congestion
Congestive
dysmenorrhea

15. may be associated with other gynaecologic symptoms, such as
dyspareunia, dysuria, abnormal bleeding, or infertility.
MANAGEMENT:
Investigation:
Treatment:
The management of secondary dysmenorrhea is mainly aimed at
treatment of the underlying disorder rather than symptomatic pain relief.
The treatment depends on the type and severity of the diseases and also
considering the age and the parity of the patient.
OTHER CAUSES:
OVARIAN DYSMENORRHEA:
Pelvic congestion or increased blood flow in the premenstrual period
resulting in marked engorgement of the vein, right ovarian vein that crosses
the ureter at right angle causes pressure on the ureter, resulting in stasis –
infection – pyelonephritis -pain.
Diagnostic
Transvaginal
sonography
Saline infusion
sonography
Therapeutic
Laparascopic
Hysteroscopy

16. REFERENCES:
 Dawood MY. Dysmenorrhea. Clin Obstet Gynecol
1990;3:168–178.
 Howard FM. Chronic pelvic pain. Obstet Gynecol
2003;101:594–611.
 Wesselmann U. Neurogenic inflammation and
chronic pelvic pain. World J Urol 2001;19:180–185.
 Dawood MY: Overall approach to the management of
dysmenorrhea. In Dawood MY, McGuire JL, Demers LM (eds):
Premenstrual Syndrome and Dysmenorrhea, p 177. Baltimore:
Urban & Schwarzenberg, 1985
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 Dawood MY: Choosing the correct therapy for dysmenorrhea.
Contemp Obstet Gynecol 19: 235, 1982
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 Dawood MY: Nonsteroidal anti-inflammatory drugs and
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17.  Dawood MY: Hormones, prostaglandins, and dysmenorrhea. In
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