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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 manifestating
as 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 ovulatory
cycles 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 dysmonorrhea
it 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 dysmonorrhea
 Age of onset is 16-25yrs
 Spasmodic pain start just prior or with the onset of
mensturation lasting 1 to 2 days
 Occurs due to excess production of prostaglandins,
vasopressin and leukotrienes
 It usually respond to COCPs and NSAIDs
 Periods remain normal in flow
 Associated 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 adenexal
tenderness 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 and
inhibiting 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 dysmonorrhea
1-NSAIDs 1st line- 80% effective
Propionic acid derivatives including
Ibuprofen and Naproxen
Fenamates including mefanamic acid
2-Oral Contraceptives – 90% effective
if NSAIDs are not effective or contraindicated
3-Follow up
some patients may require combining both drugs
Consider secondary dysmonorrhea if no improvement
with therapy
Mechanism of action
1-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 presacral
neurectomy 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 effects
1- raise the threshold for pain signals, lower the perception of
painful uterine signals
2-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
Dysmonorrhea
Dysmonorrhea

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Dysmonorrhea

  • 2. 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 manifestating as cyclical lower abdominal pain.
  • 3. 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 ovulatory cycles are established.  Secondary dysmonorrhea It is caused by underlying pathology such as endometriosis,adenomyosis,PID,IUD and polyp.
  • 4. 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
  • 5. 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.
  • 6.
  • 7.
  • 8.  Secondary dysmonorrhea it 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
  • 9.  Non-gynaecological disorders Inflammatory bowel disease Irritable bowel syndrome Urogenital disease Psychological diosorders
  • 10. Charactericstics  Primary dysmonorrhea  Age of onset is 16-25yrs  Spasmodic pain start just prior or with the onset of mensturation lasting 1 to 2 days  Occurs due to excess production of prostaglandins, vasopressin and leukotrienes  It usually respond to COCPs and NSAIDs  Periods remain normal in flow  Associated symptoms including Malaise and fatigue 85%,irritability 72%,dizziness 28%,headache 45%,lower backache 60%,diarrhea 60%,nausea,vomiting 89%  Signs are unremarkable
  • 11.  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 adenexal tenderness or a mass.
  • 12. Evaluation and diagnosis  History  Examination  Investigations including CBC,ESR,C-Reactive protein Microscopy and culture of vaginal swabs TVS Hysteroscopy Laproscopy
  • 14.  Treatment of primary dysmonorrhea is tackling the etiology with cyclooxygenase inhibitors and inhibiting 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.
  • 15. 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
  • 17. Tretment of primary dysmonorrhea 1-NSAIDs 1st line- 80% effective Propionic acid derivatives including Ibuprofen and Naproxen Fenamates including mefanamic acid 2-Oral Contraceptives – 90% effective if NSAIDs are not effective or contraindicated 3-Follow up some patients may require combining both drugs Consider secondary dysmonorrhea if no improvement with therapy
  • 18. Mechanism of action 1-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)
  • 20. 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
  • 21.  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
  • 22. 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
  • 23. Surgical treatment  There is insufficient evidence to support the routine use of surgical treatment but procedures such as laproscopic uterine nerve ablation and presacral neurectomy performed in refractory cases of dysmonorrhea.  LUNA(laproscopically uterosacral nerve ablation )  Presacral neurectomy block presacral nerve plexus
  • 24. 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
  • 25.  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
  • 26. 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
  • 27. 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
  • 28. 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
  • 29. 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 effects 1- raise the threshold for pain signals, lower the perception of painful uterine signals 2-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)
  • 30.
  • 31.  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
  • 32. 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