Dysmonorrhea

By

Dr .Nadia Sabeen

SHL

Introduction The term dysmonorrhea is derived from Greek word

Dys meaning difficult,painful meno means month and rhea means flow

Dysmonorrhea is a medical condition characterized by severe uterine pain during mensturation manifestatingas cyclical lower abdominal pain.

Types of dysmonorrhea Primary dysmonorrhea

It is defined as pain during menses in the absence of co existentent pathology.

Symptoms of primary dysmonorrhea begin few hours before the start of menses and relived during the few days of menses.

Onset is usually shortly after menarche,when ovulatorycycles are established.

Secondary dysmonorrhea

It is caused by underlying pathology such as endometriosis,adenomyosis,PID,IUD and polyp.

EPIDEMIOLOGY The reported prevalance is age related as

40% in girls aged 12 yrs

70% in girls aged 17yrs

decreases with advancing age.

Ranges from 60-93% in adolosence group

5-20% with severe dysmonorrhea

Pathophysiology Primary dysmonorrhea

The most important physiological event reported with dysmonorrhea is increased myometrial contractility with accompanying uterine ischemia which stimulate the type C afferent pain neurons.

During mensturation when there is withdrawl of progesterone, shedding of endometrium occurs and during its destruction release of inflamatory cytokines most commonl]y PGF2alpha which is myometrial stimulant and vasoconstrictor leading to pain.

The utrine contractions due to leukotrienes causing ischemia due to reduced blood supply result in uterine pain.

Secondary dysmonorrheait is cused by underlying pelvic pathology such as

Gynaecological disorders Endometriosis Adenomyosis PID Endometrial polyp Submucous fibroid IUDs Ovarian cyst Ashermans syndrome Pelvic congestive syndrome Cervical stenosis

Non-gynaecological disorders

Inflammatory bowel disease

Irritable bowel syndrome

Urogenital disease

Psychological diosorders

Charactericstics Primary dysmonorrheaAge of onset is 16-25yrsSpasmodic pain start just prior or with the onset of

mensturation lasting 1 to 2 daysOccurs due to excess production of prostaglandins,

vasopressin and leukotrienes It usually respond to COCPs and NSAIDsPeriods remain normal in flowAssociated symptoms including Malaise and fatigue

85%,irritability 72%,dizziness 28%,headache 45%,lower backache 60%,diarrhea 60%,nausea,vomiting 89%

Signs are unremarkable

Secondary dysmonorrhea

Age of onset is 30-45 yrs

Congestive Pain often progress throughout the late luteal phase and peaking with the onset of menses.

Occur due to underlying pathology and coincide with other gynaecological symptoms.

Usually resistant to OCPs and NSAIDs

Signs depend upon the cause but usually include tender,enlarged,fixed retroverted uterus with adenexaltenderness or a mass.

Evaluation and diagnosis History

Examination

Investigations including

CBC,ESR,C-Reactive protein

Microscopy and culture of vaginal swabs

TVS

Hysteroscopy

Laproscopy

Management

Treatment of primary dysmonorrhea is tackling the etiology with cyclooxygenase inhibitors andinhibiting the ovulation.

Treatment of secondary dysmonorrhea targets the cause.

The treatment strategy is based on grading the dysmonorrhea according to severity of pain and limitation of daily activities.

Evidence based treatment options for dysmonorrhea Grade A NSAIDs(other than aspirin)

Grade B&C Aspirin,Paracetamol and compound analgesics

Magnesium,Thiamine,Vit B1,B6,E,Fish oil,

High frequency TENS,Topical heat(39c)

Exercise,Japanese & chinese herbal medicines

Unknown Mirena,Surgical interruption of pelvic nerve

pathway,Acupuncture, Behavioural interventions

Magnet therapy,Vasopressin antagonists

Low frequency TENS

No benefit Spinal manipulation

Medical treatment

Tretment of primary dysmonorrhea1-NSAIDs 1st line- 80% effective

Propionic acid derivatives includingIbuprofen and NaproxenFenamates including mefanamic acid

2-Oral Contraceptives – 90% effectiveif NSAIDs are not effective or contraindicated

3-Follow upsome patients may require combining both drugsConsider secondary dysmonorrhea if no improvement

with therapy

Mechanism of action1-NSAIDs

inhibits prostaglandins production

Antagonistic action at the receptor by inhibiting the cyclooxygenase

2- Oral Contraceptives

Decrease endometrial thickness

Decrease prostaglandins through inhibition of ovulation& change the hormonal status to that of early proliferative phase(which has the lower level of PGs)

NSAIDs

Side effects of dysmonorrhea

Gastric irritation

Nausea

GIT ulceration

Increase bleeding time

Nephrotoxicity

Fenamates cause blurring of vision,headach and dizziness

Bronchospasm in patients with bronchial asthma

Hypersensitivity reactions

Autoimmune hemolytic anemia

Recommended doses of NSAIDs

Naproxen (250-275mg) 4 to 8 hourly

ibuprofen 400mg 3,4 or 6 times daily

Diclofenac 200mg/day in divided doses

Mefanamic acid 250mg 8 hourly

Nimesulide 50-100mg twice daily

Meloxicam 7.5-15mg daily

Other hormonal therapies Progestrone (depomedroxyprogestrone acetate and

levonorgestrol)

Danazol

GnRH Analogues

About 20% of women who fail to respond PG synthetase inhibitors or COCPs ,have secondary dysmonorrhea

Surgical treatment There is insufficient evidence to support the routine

use of surgical treatment but procedures such as laproscopic uterine nerve ablation and presacralneurectomy performed in refractory cases of dysmonorrhea.

LUNA(laproscopically uterosacral nerve ablation )

Presacral neurectomy block presacral nerve plexus

Treatment of secondary dysmonorrhea Treat the cause

Cervical stenosis-

Congenital

Secondary to cervical injury such as electocutery,cryocautery,conization, infection

• Pt presented with scanty menstural flow and severe cramping throughout the menstural cycle

Diagnosis – internal os scarred & impossible to pass uterine sound

Treatment –D&C

Endometriosis – ectopic endometrial tissues

Adenomyosis – endometrial tissue in the myometrium

History – severe dysmonorrhea, infertility, dyspreunia

Pelvic examination- uterine tenderness, cervical excitation, adenexal fullness

Diagnosis- laroscopy or laprotomy

Direct biopsy of vagina or cervix lesions

Treatment – medical Rx

Cauterization of endometiotic spots

Surgical removal of endometriotic cysts

Pelvic infections and adhesions PID & Pelvic abscess- adhesions- pelvic pain

History of acute episodes of pain begins with menses and continues

Pain may involve the entire abdomen

On examination- severe tenderness on palpation of uterus and cx motion(cx excitation), purulent cx discharge

Associted findings – fever and raise WBCs count & ESR

Pain due to congestion,edema and adhesions occur due to inflammatory response

treatment - appropiate antibiotics

Surgical- release of adhesions, TAH&BSO

PELVIC CONGESTION SYNDROME Engorgement of pelvic vasculature

Pain- burning or throbbiong, worst at night, and after standing for long time

On examination-vasocongestion of vagina & cervix,uterine tenderness and increase size

Diagnosis by laproscopy- congestion of uterus

Varicosities of broad ligament and pelvic side wall veins

Treatment – medroxyprogesterone acetate

TAH&BSO

Conservative treatment Herbal products and dietry supplements

Magnesium

Pyridoxine

Omega-3 fatty acid

Vitamine B1/Thiamine(100mg daily for 2 months-87% cure rate in a study)

Vitamin E- 500 units/day or 200 units twice/day

Japenese herbal medicines

Alternative remedies Exercise Topical heat treatment – 40c for 8 hours Transcutaneous electric nerve stimulation (TENS)-

altering the body ability to receive or perceive pain signals It has 2 effects1- raise the threshold for pain signals, lower the perception of

painful uterine signals2-it stimulates the release of endorphins from peripheral

nerve and spinal cord.Behavioural intrventions including hypnotherapy, imagery

, coping strategies, modification of her response to pain ( biofeedback, electromyographic training, relaxation traing)

Acupuncture

Spinal manipulation – improves spinal mobility and pelvic blood flow.

Other non hormonal therapies including

Alverine citrate – anticholinergic, antispasmodic

Transdermal glyceryl trinitrate- modulator of uterine contractiliy

Beta 2 adrenoreceptor antagonists limited due to side effects

Take home message Dysmonorrhea effects 40-70% women of reproductive

age.

Proper history and examination is necessary for diagnosis

NSAIDs are the first line therapy for primary dysmonorrhea

20% of patients not respond to NSAIDs and COCPs have secondayr dysmonorrhea

For secondary dysmonorrhea treat the cause