MENSTRUAL IRREGULARITIES- DYSMENORRHEA, PREMENSTRUAL

SYNDROME (PMS), MENORRHAGIA

INTRODUCTION

The human menstrual cycle is unique as a physiologic process in that it involves mechanisms
that change on a daily basis rather than remaining stable. This process of change is carried
out through the many intricate hormonal interactions between the hypothalamic region of the
brain, the pituitary gland, the ovaries, and to some extent, the adrenal glands and the
pancreatic islets of Langerhans The classic disorders that appearto be directly influenced by
hormonal changes that occur during the menstrual cycle are premenstrual syndrome (PMS)
and premenstrual dysphoric disorder (PMDD).Common symptoms reported by women with
PMS and PMDD include significant bloating, mood changes,depression, and emotional
lability that affect their daily activities. There is a second group of menstrual cycle–associated
disorders, the hallmark of which is regular ovulatory cycles, that causes cyclical dysfunction
of other organ systems.

Definition
Menstruation is the visible manifestation of cyclic physiologic uterine bleeding due to
shedding of the endometrium following invisible interplay of hormones mainly through
hypothalamo-pituitary ovarian axis. For the menstruation to occur, the axis must be actively
coordinated, endometrium must be responsive to the ovarian hormones (estrogen and
progesterone) and the outflow tract must be patent.

DYSMENORRHEA

INTRODUCTION

Dysmenorrhea is painful menstruation with absence of pain, generally, between menstrual

periods. It may be primary when there is no readily identifiable cause,or secondary to organic
pelvic disease. The typical age range of occurrence for primary dysmenorrhea is between 17
and 22 years, whereas secondary dysmenorrhea is more common in older women (>30years
of age). Derived from the Greek meaning diffificult monthly flow, the word dysmenorrhoea
has come to mean painful menstruation. Dysmenorrhoea can be classifified as either primary
or secondary. In the former type there is no pelvic pathology while the latter implies
underlying pathology which leads to painful menstruation.

Definition

Dysmenorrhea literally means painful menstruation. But a more realistic and practical
definition includes cases of painful menstruation of sufficient magnitude so as to
incapacitate day-to-day activities.

Types:

 Primary

 Secondary

PRIMARY DYSMENORRHEA (Spasmodic)

The primary dysmenorrhea is one where there is no identifiable pelvic pathology.

Incidence:

The incidence of primary dysmenorrhea of sufficient magnitude with incapacitation is about

15–20 percent. With the advent of oral contraceptives and non-steroidal anti-inflammatory
drugs, there is marked relief of the symptom.

Causes of pain:

 The mechanism of initiation of uterine pain in primary dysmenorrhea is difficult to

establish. But the following are too often related.
 Mostly confined to adolescents.
 Almost always confined to ovulatory cycles.
 The pain is usually cured following pregnancy and vaginal delivery.
 The pain is related to dysrhythmic uterine contractions and uterine hypoxia.
1. Psychosomatic factors of tension and anxiety during adolescence; lower the pain
threshold.
2. Abnormal anatomical and functional aspect of myometrium.
Uterine myometrial hyperactivity has been observed in cases with primary
dysmenorrhea.The outer myometrium and the subendometrial myometrium are found to be
different structurally and functionally. The subendometrial layer of myometrium is known as
Junctional Zone (JZ). There is marked hyperperistalsis of the JZ in women with
endometriosis and adenomyosis. In women with dysmenorrhea significant changes in JZ are
seen. These include irregular thickening and hyperplasia of smooth muscle and less
vascularity. This is known as Junctional zone hyperplasia. Dysperistalsis and hyperactivity of
the uterine JZ are the important mechanisms of primary dysmenorrhea.

3. Imbalance in the autonomic nervous control of uterine muscle.

There is overactivity of the sympathetic nerves → hypertonicity of the circular fibers of the
isthmus and internal os. The relief of pain following dilatation of the cervix or following
vaginal delivery may be explained by the damage of the adrenergic neurons which fail to
regenerate.

4. Role of prostaglandins

In ovulatory cycles, under the action of progesterone, prostaglandins (PGF2α, PGE2) are
synthesized from the secretory endometrium. Prostaglandins are released with maximum
production during shedding of the endometrium. PGF2α is a strong vasoconstrictor, which
causes ischemia (angina) of the myometrium. Either due to increased production of the
prostaglandins or increased sensitivity of the myometrium to the normal production of
prostaglandins, there is increased myometrial contraction with or without dysrhythmia.The
possible cause of pain owing to JZ change is shown schematically below.

5. Role of vasopressin: There is increased vasopressin release during menstruation in women

with primary dysmenorrhea. This explains the persistence of pain in cases even treated with
antiprostaglandin drugs. The mechanism of action is yet to be explored. Vasopressin
increases prostaglandin synthesis and also increases myometrial activity directly. It causes
uterine hyperactivity and dysrhythmic contractions →ischemia and hypoxia → pain.

6. Endothelins causes myometrial smooth muscle contractions, specially in the

endomyometrial Junction (JZ). Endothelins in endometrium can induce PFG2α. Local
myometrial ischemia caused by endothelins and PGF2α aggravate uterine dysperistalsis and
hyperactivity.

7. Platelet activating factor (PAF) is also associated with the etiology of dysmenorrhea as
its concentration is found high. Leukotrienes and PAFs are vasoconstrictors and stimulate
myometrial contractions. Pain is spasmodic and confined to lower abdomen; may radiate to
the back and medial aspect of thighs. Systemic discomforts like nausea, vomiting, fatigue,
diarrhea, headache and tachycardia may be associated. It may be accompanied by vasomotor
changes causing pallor, cold sweats and occasional fainting. Rarely, syncope and collapse in
severe cases may be associated.Abdominal or pelvic examination does not reveal any
abnormal findings. For detection of any pelvic abnormalities, ultrasound is very useful and it
is not invasive.

Treatment: General measures include improvement of general health and simple

psychotherapy in terms of explanation and assurance. Usual activities including sports are to
be continued. During menses, bowel should be kept empty; mild analgesics and
antispasmodics may be prescribed. Habit forming drugs such as pethidine or morphine must
not be prescribed. With these simple measures, the pain is relieved in majority.

Severe cases:

 Drugs
 Surgery

DRUGS: The drugs used are —

 Prostaglandin synthetase inhibitors.

 Oral contraceptives (combined estrogen and progestogen).

 Prostaglandin synthetase inhibitors (PSI)

These drugs not only reduce the prostaglandin synthesis (by inhibition of cyclo-
oxygenase enzyme) but also have a direct analgesic effect. Intrauterine pressure is
reduced significantly. Any of the preparations listed in the table can be used orally for 2–
3 days starting with the onset of period. The drug should be continued for 3–6 cycles.

 Fenamate group — mefenamic acid 250–500 mg 8 hourly or flufenamic acid 100–

200 mg 8 hourly.
 Propionic acid derivatives —

ibuprofen 400 mg 8 hourly or naproxen 250 mg 6 hourly.

Indomethacin 25 mg 8 hourly.

COMMONLY USED NSAIDs

Newer drugs NSAIDs inhibit two different isoforms of the enzyme cyclo-oxygenase:

COX–1 and COX–2. Selective inhibitors of the enzyme COX-2 may have similar analgesic
efficacy but fewer side effects. Transdermal use of smooth muscle relaxant glyceryl trinitrate
is also used currently. The suitable cases are—comparatively young age and having
contraindications to ‘pill’. The contraindications of its use include allergy to aspirin, gastric
ulceration and history of asthma.
ORAL CONTRACEPTIVE PILLS:

The suitable candidates are patients

(i) Wanting contraceptive precaution,

(ii) With heavy periods and

(iii) Unresponsive or contraindications to anti-prostaglandin drugs. The pill should be

used for 3–6 cycles.

DYDROGESTERONE: It does not inhibit ovulation but probably interferes with ovarian
steroidogenesis. The drug should be taken from day 5 of a cycle for 20 days. It should be
continued for 3–6 cycles.If the above protocol fails, laparoscopy is indicated to find out any
pelvic pathology to account for pain, the important one being endometriosis.

SURGERY: Transcutaneous electrical nerve stimulation (TENS) has been used to relieve
dysmenorrhea. Results are not better than that of analgesics.

SURGICAL PROCEDURES: Laparoscopic uterine nerve ablation (LUNA) for primary

dysmenorrhea has not been found beneficial. Laparoscopic presacral neurectomy is done to
cut down the sensory pathways (via T11–T12) from the uterus. It is not helpful for adnexal
pain (T9–T10) as it is carried out by thoracic autonomic nerves along the ovarian vessels. As
such its role in true dysmenorrhea is questionable.

DILATATION OF CERVICAL CANAL: It is done under anesthesia for slow dilatation of

the cervix to relieve pain by damaging the sensory nerve endings. It is not commonly done.
Late sequela may be cervical incompetence.

SECONDARY DYSMENORRHEA (Congestive)

Secondary dysmenorrhea is normally considered to be menstruation — associated pain

occurring in the presence of pelvic pathology.

Causes of pain: The pain may be related to increasing tension in the pelvic tissues due to
pre-menstrual pelvic congestion or increased vascularity in the pelvic organs.

Common causes of secondary dysmenorrhea:

Cervical stenosis, chronic pelvic infection, pelvic endometriosis, pelvic adhesions,

adenomyosis, uterine fibroid, endometrial polyp, IUCD in utero and pelvic congestion.
Obstruction due to mullerian malformations are the other causes.
Patient profile: The patients are usually in their thirties; more often parous and unrelated to
any social status.

Clinical features: The pain is dull, situated in the back and in front without any radiation. It
usually appears 3–5 days prior to the period and relieves with the start of bleeding. The onset
and duration of pain depends on the pathology producing the pain. There is no systemic
discomfort unlike primary dysmenorrhea. The patients may have got some discomfort even in
between periods. There are symptoms of associated pelvic pathology. Abdominal and vaginal
examinations usually reveal the offending lesion. At times, the lesion is revealed by
laparoscopy, hysteroscopy or laparotomy

Treatment: The treatment aims at the cause rather than the symptom. The type of treatment
depends on the severity, age and parity of the patient.

 Ovarian dysmenorrhea
 bicornuate uterus
 unilateral location of pelvic endometriosis
 small fibroid polyp near one cornua
  right ovarian vein syndrome
 colonic or cecal spasm

Ovarian Dysmenorrhea

Right ovarian vein syndrome: Right ovarian vein crosses the ureter at right angle. During
premenstrual period, due to pelvic congestion or increased blood flow, there may be marked
engorgement in the vein → pressure on ureter → stasis → infection →pyelonephritis → pain.

MITTELSCHMERZ’S SYNDROME

(Ovular Pain)

Ovular pain is not an infrequent complaint. It appears in the midmenstrual period. The pain is
usually situated in the hypogastrium or in either iliac fossa. The pain is usually located on one
side and does not change from side to side according to which ovary is ovulating. Nausea or
vomiting is conspicuously absent. It rarely lasts more than 12 hours. It may be associated
with slight vaginal bleeding or excessive mucoid vaginal discharge.The exact cause is not
known. The probable factors are:

(i) Increased tension of the Graafian follicle just prior to rupture,

(ii) Peritoneal irritation by the follicular fluid following ovulation and
(iii) Contraction of the tubes and uterus.

Treatment is effective with assurance and analgesics. In obstinate cases, the cure is absolute
by making the cycle anovular with contraceptive pills.
PREMENSTRUAL SYNDROME (PMS)

(Syn : Premenstrual Tension)

INTRODUCTION

Premenstrual syndrome (PMS), also described as premenstrual tension (PMT), is a symptom

complex recognized primarily by cyclic changes associated with ovulatory cycles. It occurs
7–14 days prior to menstruation and spontaneously resolves after menses. It is frequently
encountered in middle aged women. It is important for two reasons, firstly because the
symptoms of PMT are responsible for socioeconomic loss and secondly because of associated
legal and women’s rights issues that have arisen in conjunction with personal account ability
during the premenstrual period. It comprises physical, psychological and behavioural changes
not associated with organic lesion. It is prevalent in 5% women.

DEFINITION

Premenstrual syndrome (PMS) is a psychoneuroendocrine disorder of unknown etiology,

often noticed just prior to menstruation. There is cyclic appearance of a large number of
symptoms during the last 7–10 days of the menstrual cycle.

INCIDENCE

As many as 80% of regularly ovulating women will experience some degree of physical
and psychological premenstrual symptomatology. These mild “moliminal” symptoms are
normal, and characteristic of ovulatory cycles. About 5-10% of these women have
moderate symptoms that are disruptive to daily activities and are said to have PMS.In less
than 5% of women, these symptoms are so severe that they seriously interfere with usual
daily functioning and personal relationships. When these women meet the criteria
outlined, they may be diagnosed with PMDD.
It should fulfill the following criteria (ACOG)

 Not related to any organic lesion.

 Regularly occurs during the luteal phase of each ovulatory menstrual cycle.
 Symptoms must be severe enough to disturb the life style of the woman or she
requires medical help.
 Symptom-free period during rest of the cycle.
 When these symptoms disrupt daily functioning they are grouped under the name
premenstrual dysphoric disorder (PMDD).

The Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric

Association for PMDD
 Although the DSM-IV definition of PMDD specifies that this is not just an exacerbation
of another disorder, the dividing line between PMDD and other neuropsychiatric
disorders is not so clear cut. For example, 46% of PMDD patients have a history of a
prior major depressive episode. Moreover, patients with PMDD and clinical depression
share similar alterations on a sleep electroencephalogram (EEG), and they are both
responsiveto the selective serotonin reuptake inhibitor (SSRI) antidepressants.

PATHOPHYSIOLOGY:

The exact cause of PMS is not known. It has been postulated that it represents a syndrome
which is the result of multiple biochemical abnormalities. Amongst these, the following have
been implicated:

(i) Either there is altered estrogen : progesterone ratio or diminished progesterone

level.
(ii) Increased carbohydrate intolerance in the luteal phase;
(iii) Pyridoxine deficiency—this vitamin plays a role in oestrogen synthesis and also in
dopamine and serotonin production;
 (iv) Increased production of vasopressin, aldosterone, prolactin and systemic
prostaglandins which adversely affect renal function and contribute to fluid
retention and bloating; and
(v) Fluctuations in opiate peptide concentrations affecting endorphin levels. However,
biochemical estimations do not bear these out. Hence, at present it is not yet clear
whether PMS is an abnormal response to normal hormonal fluctuation or a result
of hormonal abnormalities. A woman with hysterectomy but conservation of
ovaries may also suffer from PMT suggesting that the ovarian hormones have a
role in PMT.
(vi) Low level of b-endorphins (neurotransmitters) in the brain and low level of
serotonin are probably responsible for psychiatric disorders.
(vii) Genetic predisposition is also recognized in a few cases.

CLINICAL FEATURES:

 PMS is more common in women aged 30–45. It may be related to childbirth or a

disturbing life event.
 The syndrome may be mild, moderate or severe. Symptoms of PMS are myriad and
not associated with organic lesion in the pelvis.
 The classic description includes increasing breast tenderness, abdominal bloating,
headache, sleeplessness, fatigue, emotional lability, mood swings and depression,
irritability, fluid retention and weight gain beginning 7–14 days prior to menses. As
menstruation approaches, psychological abnormalities like irritability and hostility
increase.
 The dominant symptom in different groups varies from anxiety, to depression, to fluid
retention, bloating, headache and breast pain (mastodynia), to increased appetite and
craving for sweet foods.
 Five per cent suffer from severe symptoms which influence daily activity. The body
weight increases by 1 kg and breast volume by 20% due to oedema and increased
vascularity.
 PMT does not occur before puberty, during pregnancy or after menopause. It may
however occur if the post-menopausal woman goes on hormone replacement therapy
(HRT).
DIAGNOSIS

Diagnosis depends on history and careful questioning. Temporal correlation of symptoms

with the premenstrual phase of the cycle as documented in a menstrual diary helps to arrive at
a rational diagnosis. No organic pelvic lesion is detected, and no definite test is available to
confirm the diagnosis.

MENSTRUAL DIARY

 Because the etiology of PMS and PMDD is not clear, no definitive physical
examination or laboratory markers are available to aid in diagnosis.
 At present, the definitive diagnosis of PMS and PMDD hinges on documentation of
the relationship of the patient’s symptoms to the luteal phase.
 Prospective documentation of symptoms can be accomplished using a menstrual diary
in two or more consecutive menstrual cycles.
 The patient is asked to monitor her symptoms and the pattern of menstrual bleeding
for two or more cycles.
 For PMS, she needs only to have one of the listed symptoms but must have a
symptom-free interval.
 For PMDD, the patient is asked to also monitor the severity of symptoms.
 She must demonstrate 5 of the listed 11 symptoms , one of which must be a core
symptom. She must also demonstrate a symptom-free follicular phase. If her
 symptoms persist during the follicular phase but are less severe, luteal phase
worsening of a different disorder (sometimes called entrainment) should be
considered.

TREATMENT

As the etiology is multifactorial and too often obscure, various drugs are used either on
speculation or empirically with varying degrees of success. Life style modification and
congnitive behavior therapy are important steps.

GENERAL

NONPHARMACOLOGICAL:

 Diet recommendations emphasize eating fresh rather than processed foods. The
patient is encouraged to eat more fruits and vegetables and minimize the intake of
refined sugars and fats.
 Minimizing salt intake may help with bloating, and eliminating caffeine and alcohol
from the diet can reduce nervousness and anxiety.
 None of these therapies have shown statistically significant improvements in PMS
and PMDD, but they are reasonable, benign, and a good part of general health
improvement.
 In some studies, these interventions have demonstrated trends toward improvement.
Clearly, they yield low risks and are generally healthful behaviors.
 Lifestyle interventions that have demonstrated significant improvement in symptoms
include aerobic exercise and calcium carbonate and magnesium supplementation.
 Aerobic exercise, as opposed to static (e.g., weightlifting) exercise, has been found to
be helpful in some patients, possibly by increasing endogenous production of
endorphins.
 Calcium decreases water retention, food cravings, pain, and negative affect compared
with placebo.
 Other interventions have been studied but demonstrate conflicting results. These
include vitamins E and D and chaste tree berry extract as well as relaxation therapy,
cognitive therapy, and light therapy. Many of these therapies have no untoward side
effects and can be considered for certain patients.
 Studies have shown that vitamin B6 supplementation has limited clinical benefit.
Patients should be cautioned that dosages in excess of 100 mg/day may cause medical
 harm, including peripheral neuropathy. Studies of evening primrose oil demonstrate
no benefit.
 Alternative therapies include meditation, aromatherapy, reflexology, acupuncture,
acupressure, and yoga. Further research is warranted in these areas.

PHARMACOLOGIC TREATMENT

In addition to lifestyle changes, behavioral therapies, and dietary supplementation, some

pharmacologic agents have been shown to provide symptomatic relief. Nonsteroidal anti-
inflammatory agents have been found in controlled trials to be useful in PMS patients
with dysmenorrhea, breast pain, and leg edema but not useful in treating other aspects of
PMS. This effect is possibly related to prostaglandin production in various sites in the
body. Spironolactone decreases bloating but does not relieve other symptoms.

(a) Tranquilizers or antidepressant drugs, may be of help logically.

(b) Pyridoxine – 100 mg twice daily is helpful by correcting tryptophan metabolism

specially following ‘pill’ associated depression.

(c) Diuretics in the second half of the cycle – Frusemide 20 mg daily for consecutive 5
days a week reduces fluid retention.

(d) Anxiolytic agents are found to be helpful to women having persistent anxiety.
Alprazolam 0.25 mg, bid) is given during the luteal phase of the cycle.

(e) Selective Serotonin Reuptake Inhibitors (SSRI) and Noradrenaline Reuptake

Inhibitors (SNRI) are found to be very effective. Fluoxetine is an antidepressant that
inhibits neuronal uptake of serotonin (SSRI). A single oral dose of 20 mg was found to
improve the psychiatric and behavioral symptoms significantly. The drugs are usually
prescribed at least two days prior to the onset of symptoms and to be continued till
menstruation starts.

Other drugs used are: Sertaline (50 mg/day) and Venlafaxine.

HORMONES:

Any one of the following drugs is to be prescribed:

 Oral contraceptive pills: The idea is to suppress ovulation and to maintain

an uniform hormonal milieu. The therapy is to be continued for 3–6 cycles.
 Newer OCPs contain progestin drospirenone. It has antimineralocorticoid and
antiandrogenic properties. Drospirenone containing OCPs are found to have
better control of symptoms.
 Progesterone is not effective in treating PMS.
 Levonorgestrel intrauterine system (IUS) had been used to suppress
ovarian cycle.
 Spironolactone: It is a potassium sparing diuretic. It has anti-
mineralocorticoid and anti-androgenic effects. It is given in the luteal phase
(25–200 mg/day). It improves the symptoms of PMDD.
 Bromocriptine: 2.5 mg daily or twice daily may be helpful, at least to relieve
the breast complaints.

SUPPRESSION OF OVARIAN CYCLE:

Suppression of the endogenous ovarian cycle can be achieved by:
 Danazol 200 mg daily is to be adjusted so as to produce amenorrhea. Barrier method
of contraception should be advised during the treatment.
 GnRH analogues— The gonadal steroids are suppressed by administration of GnRH
agonist for 6 months (medical oophorectomy). GnRH analogues in PMS are used:
(i) To assess the role of ovarian steroids in the aetiology of PMS.
(ii) This can also predict whether bilateral oophorectomy would be of any help or
not. The preparations and doses used are as given.
 Goserelin (Zoladex): 3.6 mg is given subcutaneously at every 4
weeks.
 Leuprorelin acetate (Prostap):3.75 mg is given by SC or IM at
every 4 weeks.
 Triptorelin (Decapeptyl) : 3 mg is given IM every 4 weeks.
Results of GnRH agonist therapy are dramatic.
GnRH agonist therapy is combined with estrogen progestin “add-back” to
combat the hypoestrogenic symptoms.

OOPHORECTOMY
In established cases of primary PMS with recurrence of symptoms and approaching
to menopause, hysterectomy with bilateral oophorectomy is a last resort.
MENORRHAGIA (Syn:Hypermenorrhea)

INTRODUCTION:
 The term ‘menorrhagia’ is from the Greek word, men meaning ‘menses’ and rrhagia
meaning ‘burst forth’. Menorrhagia denotes cyclic regular bleeding which is
excessive in amount or duration.
 It is generally caused by conditions affecting the uterus or its vascularity, rather than
any disturbance of function of the hypothalamic–pituitary–ovarian (H-P-O) axis.
 Whenever the uterine endometrial surface is enlarged, the bleeding surface is
increased, contributing to excessive bleeding. Such conditions prevail in uterine
fibroids, adenomyosis, uterine polyps, myohyperplasia and endometrial hyperplasia.
 Menorrhagia is also seen in women with increased uterine vascularity such as in
chronic pelvic inflammatory disease and pelvic endometriosis. The uterus is often
retroverted in position with restricted mobility. Such a uterus tends to be bulky and
congested. The presence of an IUCD often leads to heavy and prolonged bleeding.
 Lastly, menorrhagia may be the result of bleeding disorders like Von Willebrand’s
disease or an arteriovenous aneurysm.
 A normal menstrual blood loss is 50 to 80 mL, and does not exceed 100 mL. In
menorrhagia, the menstrual cycle is unaltered, but the duration and quantity of the
menstrual loss are increased.
 Menorrhagia is essentially a symptom and not in itself a disease. It affects 20–30% of
women at sometime or other with significant adverse effects on the quality of life in
terms of anaemia, cost of sanitary pads and interference with day-to-day activities.
Several causes may prevail in a few cases, and attribute to excess bleeding. The
underlying cause may be difficult to detect, in a few cases.

NORMAL CONTROL OF MENSTRUAL BLEEDING

Once the menstrual bleeding starts, the platelet aggregation forms clots in the opened vessels.
Prostaglandin F2a(PGF2a) causes myometrial contractions and constricts the endometrial
vessels. The repair and epithelial regeneration begin on the 3rd and 4th day of period, by the
growth of epithelial cells from the open endometrial glands aided by the vascular endothelial,
epidermal and fibroblast growth factors. In excessive bleeding with regular menstrual cycles,
the H-P-O axis is intact, but endometrial changes get altered. It is observed that, in these
cases, PGE2 (prostacyclin), which is a local vasodilator is increased as compared to PGF2a in
the endometrial tissue.
DEFINITION
Menorrhagia is defined as cyclic bleeding at normal intervals; the bleeding is either excessive
in amount (>80 mL) or duration (>7 days) or both. The term menotaxis is often used to
denote prolonged bleeding.

CAUSES:
Menorrhagia is a symptom of some underlying pathology—organic or functional.
ORGANIC
1. PELVIC
Due to congestion, increased surface area, or hyperplasia of the endometrium
 Fibroid uterus
 Adenomyosis
 Pelvic endometriosis
 IUCD inutero
 Chronic tubo-ovarian mass
 Tubercular endometritis (early cases)
 Retroverted uterus—due to congestion
 Granulosa cell tumor of the ovary
Systemic:
 Liver dysfunction—failure to conjugate and thereby inactivates the estrogens.
 Congestive cardiac failure.
 Severe hypertension.
Endocrinal
 Hypothyroidism.
 Hyperthyroidism.

HEMATOLOGICAL
 Idiopathic thrombocytopenic purpura.
 Leukemia. von Willebrand’s disease.
 Platelet deficiency.
 Emotional upset
Functional
 Due to disturbed hypothalamo-pituitary-ovarian endometrial axis. menorrhagia
Dysfunctional uterine bleeding
Fibroid uterus
Adenomyosis
Chronic tubo-ovarian mass

DIAGNOSIS
 Long duration of flow, passage of big clots, use of increased number of thick sanitary
pads, pallor, and low level of hemoglobin give an idea about the correct diagnosis and
magnitude of menorrhagia. Menorrhagia patients require to be completely
investigated. Besides physical examination, the following tests are advised:
 Complete haemogram.
 Bleeding time and clotting time.
 Thyroid profile as indicated.
 Pelvic sonography—sonosalpingography.
 Diagnostic hysteroscopy.
 Diagnostic laparoscopy.
 Endometrial study by ultrasound and curettage.
 Sonosalpingography can delineate a submucous fibroid clearly.
 Pelvic angiography is required when the cause of menorrhagia is not detected
by other means. This shows varicosity and arteriovenous fistula.

TREATMENT
 The definitive treatment is appropriate to the cause for menorrhagia.
 Management consists of the following:
 General measures to improve the health status of the patient. Advice regarding
proper diet, adequate rest during menses, oral administration of haematinics,
vitamins and protein supplements and to maintain a menstrual calendar noting
duration and extent of blood loss.
 Treat the cause.
 In women suffering from menorrhagia, consider the following:
  In ovulatory cycles, oral nonsteroidal anti-inflammatory drugs
(NSAIDs) like mefenamic acid 500 mg t.i.d along with antacids.
 Other drugs in this category include naproxen, ponstan and ibuprofen.
Blood loss is reduced by 30–40%. These drugs are effective in
ovulatory bleeding and in IUCD users. They are antiprostaglandins
and inhibit cyclo-oxygenase activity. They decrease the menstrual
bleeding, but have no effect on the duration of menstrual bleeding.
These drugs should be taken only during menstruation, which is an
advantage, over cyclical hormone therapy.
 Cyclic oral contraceptive pills.
 Progestogens in endometrial hyperplasia.
 Mirena IUCD.
 Minimal invasive surgery includes endometrial thermal ablation,
endometrial resection and others
 Hysterectomy in selected cases.
 n GnRH—It is not effective in acute bleeding as it takes 4 weeks to
cause effect.
In women manifesting obvious pathology, corrective measures for the same are called for,
depending on her age and the desire for retaining menstrual and childbearing functions.
Therapeutic measures include:
 Removal of an intrauterine contraceptive device if medical therapy fails.
 Myomectomy/hysterectomy for uterine fibroids.
 Wedge resection/hysterectomy for adenomyosis of the uterus.
 Laparoscopic lysis of adhesions for chronic PID.
 Electrocautery or laser vaporization of endometriosis and drainage of chocolate cysts
in pelvic endometriosis.
 Hysterectomy with or without removal of the adnexa according to the age and the
individual needs of the patient.
 In patients suffering from bleeding disorders, a haematologist’s opinion should be
sought.
 Uterine artery embolization in varicose vessels.
 Von Willebrand’s disease; intravenous desmopressin..
 

CONCLUSION

Some menstrual irregularities can be caused by serious, even life-threatening conditions, such
as uterine cancer. Seek prompt medical care if you have menstrual irregularities, such as
heavy menstrual periods or a lack of menstrual periods. Early diagnosis and treatment of
menstrual irregularities reduces the risk of serious complications, such as infertility and
metastatic uterine cancer.

Prevalence of premenstrual syndrome and its association with psychosocial and lifestyle
variables: a cross-sectional study from Palestine

Background

Premenstrual Syndrome (PMS) is a very common problem with symptoms that can
negatively affect normal daily life. This cross-sectional study aimed to investigate the
prevalence of PMS symptoms and their relationship with psychosocial status and lifestyle of
female students at An-Najah National University in Palestine. A sample of 398 female
students was randomly selected to participate in the study. Arabic Premenstrual Scale (A-
PMS) was used for PMS assessment. Psychosocial variables were determined using the
DASS-21 Arabic version, and dietary habits were measured using a 24 item self-reported
questionnaire. Data was analyzed by one-way ANOVA and Chi-square tests using SPSS
software version 23.

Results

The 398 participants (100%) suffered from some kind of PMS symptoms; 398 (100%) had
physical symptoms, 397 (99.7%) had psychological symptoms, and 339 (85.2%) had
behavioral PMS symptoms. All PMS symptoms were significantly associated with student
psychosocial status (p < 0.01). Preferring a certain type of food during menstruation was
significantly related to psychological PMS symptoms (p < 0.001), and physical symptoms (p 
< 0.01). Following a diet was significantly related to physical symptoms (p < 0.05) and
behavioral symptoms (p < 0.001). Moreover, drinking herbal tea was significantly related to
physical symptoms (p < 0.001) and behavioral symptoms (p < 0.05).

Conclusion

The findings of the study revealed a relatively high prevalence of PMS syndrome with a
significant relationship with dietary habits and psychosocial status.
KATHARINE KOLCABA

THEORY OF COMFORT

 “Comfort is an antidote to the stressors inherent in health care situations today, and
when comfort is enhanced, patients and families are strengthened for the tasks ahead.
Also, nurses feel more satisfied with the care they are giving.”
 Patient comfort exists in three forms: relief, ease, and transcendence. These comforts
can occur in four contexts: physical, psychospiritual, environmental, and
sociocultural.
 As a patient’s comfort needs change, the nurse’s interventions change, as well.

BIBILIOGRAPHY

 K. Hiralal. Dc Dutta’s Textbook Of Gynecology Including Contraception:6th Edition,

Jaypee Brothers Medical Publishers (P) Ltd;Pg 334-340.
 D. Keith Edmonds. Dewhurst’s Textbook Of Obstetrics & Gynaecology. 7th
Edition:Blackwell Publishing;Pg 554-570.
 Howkins & Bourne Shaw’s Textbook of Gynaecology.16th edition:elseveir;pg778-
790.
 Hacker & Moore’s. Essentials Of Obstetrics & Gynecology.6th Edition.Elseveir;Pg
678-680.
 Abu Alwafa, R., Badrasawi, M. & Haj Hamad, R. Prevalence of premenstrual
syndrome and its association with psychosocial and lifestyle variables: a cross-
sectional study from Palestine. BMC Women's Health 21, 233 (2021).
https://doi.org/10.1186/s12905-021-01374-6