Dysmenorrhea affects over 50% of all postpubescent women, 5% are incapacitated for 1-3 days each month.
Primary dysmenorrhea is painful menses without evidence of an organic lesion or cause, usually brief, and worst on the first day of menstruation. This type of dysmenorrhea is seen in ovulatory menstrual cycles, usually within five years of menarche, and improves with age. Most theories center around excess prostaglandin PGF2alpha, resulting in smooth muscle contraction. The role of estrogen and progesterone is unclear: estrogen is a stimulator of uterine activity, and progesterone is an inhibitor. Yet women with high levels of estrogen, such as those with anovulatory cycles and obesity, typically do not experience much dysmenorrhea.
Treatment of primary dysmenorrhea usually is aimed at prostaglandin inhibition or suppression of cycles. Other non-specific measures such as heat, mild analgesics, and exercise should be encouraged, but narcotics are not used. Does the patient need contraception: Does she have other complains which make suppression of menses favorable?
Secondary dysmenorrhea accounts for 20% of all dysmenorrhea, usually develops later than primary, and is due to an underlying condition. Treatment is aimed at correcting the underlying condition:
adenomyosis: gland-like growth into myometrium
endometriosis: ectopic endometrial tissue
fibroids: (covered separately)
intrauterine devices (IUD)
endometritis: chronic infection of uterus
congenital uterine anomalies: menstrual flow may lack an outflow tract
other: ovarian cysts, pelvic varicosities
Abnormal Uterine Bleeding is defined as any bleeding which is considered excessive in frequency, duration, or amount by the patient, and as such should be evaluated. The pathophysiology involves hormonal balances, pregnancy, structural abnormalities, and cancer.
If the patient is ovulatory, causes include:
If the patient is anovulatory, causes include:
dysfunctional uterine bleeding (DUB)
extrinsic hormone effects
perimenopausal bleeding: hyperplastic, neoplastic
Dysfunctional and perimenopausal bleeding merit further discussion. DUB is the result of persistent anovulation where the endometrial lining does not shed in a synchronous fashion.
Consider exogenous or endogenous sources of excess estrogen, such as peripheral conversion
of androgens to estrone in obese individuals. Unopposed estrogen can lead to endometrial
hyperplasia: we usually sample the endometrial lining in women aged 35 years or older who
experience DUB. Perimenopausal bleeding is also anovulatory bleeding and should be
evaluated for hyperplasia.
The evaluation includes a pelvic exam, and may include an endometrial biopsy. Hysteroscopy
visualizes the endometrial lining to identify polyps, fibroids, anomalies, and direct biopsies.
Blood work includes a hematocrit, thyroid studies, prolactin, and pituitary hormones (LH,
FSH) in select individuals. Don't forget pregnancy as a cause of abnormal uterine
bleeding! To biopsy or hysteroscope such a patient would be disastrous.
Treatment of abnormal uterine bleeding:
If the abnormality is anatomic, we surgical remove polyps or fibroids. Antibiotic therapy is used for chronic endometritis, or an IUD may be removed. Occasionally the patient is considered for endometrial ablation or hysterectomy.
If the abnormality is anovulation, exogenous progestins, estrogens, or combination therapy is used.
acute severe bleeding is an emergency, seen in menarcheal girls and perimenopausal women. Stabilize the patient with fluids, consider pregnancy and bleeding dyscrasias. IV Premarin (conjugated equine estrogens) is used, and is thought to stabilize the spiral arteries of the endometrium. A dilation and curettage (D&C) in the operating room is rarely used.
in less severe cases, a "chemical D&C" is accomplished with a progesterone shot, 10 days of medroxyprogesterone 10 mg, or oral contraceptive pills in high doses (2-4 per day.) The progesterone effect is to shut down estrogen receptors, and withdrawal from progesterone triggers the shedding of the endometrium.
chronic anovulatory bleeding may be managed by observation, oral contraceptives, cyclic progesterone, or ovulation induction. If hyperplasia has been diagnosed in high risk individuals, progesterone must be used to reverse the effects of chronic anovulation. Only hyperplasia with atypia is considered a premalignant lesion.
Premenstrual Syndrome (PMS)
This is felt to be an exaggerated presentation of molimina, the symptoms that many women experience in the luteal phase of the cycle and which accompany ovulatory cycles. An important attribute is that symptoms are found in the luteal phase, and absent in the postmenstrual week. Although many hypotheses exist, the etiology is essentially unknown.
Several key points in PMS:
all that cycles is not PMS. Some conditions vary with the menstrual cycles, including thyroid size, basal body temperature, and alcohol metabolism. Other conditions are exacerbated, but not caused by phases of the menstrual cycles: migraine, seizure disorders, asthma, genital herpes, and even angina. Mood disorders may commonly be exacerbated in the luteal phase.
all premenstrual changes may not be PMS. Molimina should not be labelled as PMS unless they are severe enough to disrupt daily life and family interactions, or affect alcohol, drug use, or suicidal thoughts.
PMS may be more than one entity. It is unclear why some women have emotional effects (depression, emotional lability),while others experience physical effects (water retention, pain, breast tenderness.)
Evaluation is usually made by history alone; there are no specific physical findings or laboratory abnormalities. A calendar of symptoms should clearly demonstrate a luteal phase effect, with absence of symptoms after menstruation.
Management is empiric, since the etiology is unknown. Even recent textbooks of gynecology suggest that most women suffering from PMS are somehow "causing it" and that successful treatment depends on a "responsive and cooperative patient who wants to get better." Overcoming these stigma and acknowledging symptoms as real pathology is an important part of therapy.
Stress urinary incontinence is the loss of urine with coughing, sneezing, laughing, or other increases in intra-abdominal pressure. The pathophysiology is incomplete transmission of intraabominal pressure to the bladder neck (where the bladder meets the urethra.)
baseline bladder pressure = 10 cm H2O
cough bladder pressure = 100 cm H2O
baseline urethral pressure = 50 cm H2O
1. Good transmission, no stress incontinence
2. Poor transmission,stress incontinence
10 + 100
10 + 100
50 + 100
50 + 50
Evaluation includes history, exam excluding large postvoid residuals, and hypermobility of the bladder neck. Because symptoms may be confusing or mixed, further urodynamic testing may be needed. A cystometrogram (CMG) measures pressures in the bladder, urethra, and vagina, and can distinguish stress from urge incontinence.
Treatment is driven by the patient's needs: mild-to-moderate stress incontinence is treated with:
pelvic floor exercises
devices to stabilize the bladder neck
alpha-agonists to increase intraurethral resting pressure.
Moderate-to-severe stress incontinence is often treating by surgery aimed at supporting and stabilizing the bladder neck. This is the only type of incontinence to improve with surgery; compromised voiding is a common adverse outcome.
Urge incontinence (detrusor instability, unstable bladder) is the sudden loss of urine associated with a uninhabitable detrusor contraction, mediated parasympathetically. Clinically, patients experience urgency, frequency, nocturia, and nocturnal enuresis. Common antecedents are listening to running water, or arriving home and unlocking the door. Evaluation is as above, but looking for neurologic abnormalities. A bladder diary may show excess fluid output, small voided volumes, etc.
Treatment of urge incontinence is NOT surgical. Patients are offered bladder retraining, a timed-void behavior modification. Some patients need anticholinergic agents such as oxybutynin (2.5-5 mg t.i.d.) or hyoscyamine 0.125 q 4 hours, or 0.375 b.i.d.
This condition is seen in 20-30% of women 35 years and older. It is often a symptomatic and should be followed clinically. Uterine enlargement should be noted, and the adnexa may need to be evaluated with ultrasound because the size of the uterus limits palpation of other structures. Because the condition is common and malignant degeneration is rare (less than 0.2%), it is not necessary to perform ultrasound or endometrial sampling. The tumors are smooth muscle, and are estrogen responsive. Therefore, most fibroids will regress postmenopausally even with hormone replacement therapy.
Bleeding may result from submucosal fibroids: the endometrium is distorted over the mass, and normal mechanisms of shedding are compromised. In women with abnormal uterine bleeding unresponsive to hormonal management, a hysteroscopy or ultrasound may reveal a submucosal fibroid. Hysteroscopic resection or hysterectomy is the usual treatment after failure of medical management. GnRH agonists may be used short-term to shrink fibroids for easier surgical management. Fibroids which outgrow their blood supply may become painful. Myomectomy is usually reserved for women who wish to preserve fertility, since other fibroids are likely to grow. The most common clinical manifestation of fibroids is discomfort due to the mass itself. Although hysterectomy was previously recommended for enlargement the size of a twelve week pregnancy or greater, now most fibroids are followed clinically until menopause.