Disclosures The author reports no conflicts of interest and no inducements were made by any commercial entity to submit this article.
A case study and comprehensive differential diagnosis and care plan for the three Ds of women's health: Primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia
Article first published online: 3 SEP 2010
©2010 The Author Journal compilation ©2010 American Academy of Nurse Practitioners
Journal of the American Academy of Nurse Practitioners
Volume 22, Issue 10, pages 513–522, October 2010
How to Cite
Stoelting-Gettelfinger, W. (2010), A case study and comprehensive differential diagnosis and care plan for the three Ds of women's health: Primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia. Journal of the American Academy of Nurse Practitioners, 22: 513–522. doi: 10.1111/j.1745-7599.2010.00544.x
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- Issue published online: 11 OCT 2010
- Article first published online: 3 SEP 2010
- Received: December 2008;accepted: July 2009
- Women's health;
- young adult women;
- sexual health;
- human papilloma virus (HPV);
- patient education;
- primary care
Abstract Purpose: To provide a case study for the discussion, diagnosis, management, and comprehensive plan of care for primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia for the advanced practice registered nurse (APRN) working in primary care.
Data sources: Selected text, research, clinical articles, and personal communication with expert APRNs.
Conclusions: Three of the most commonly presenting women's health related conditions include primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia. These conditions can present a challenge in developing an accurate differential diagnosis and appropriate plan of care. This article presents the reader with a detailed case study that provides an analysis of each potential differential diagnosis with rationale. A recommended diagnostic and therapeutic plan of care is included for the reader's review.
Implications for practice: If left untreated, primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia can result in pain, suffering, and impaired fertility and sexual function. Patients frequently experience symptoms for months to years prior to accurate diagnosis.
Ms. S is a 20-year-old healthy female with a 2-year history of dysmenorrhea with onset of symptoms at age 18, 4 years after menarche. Past medical history included a diagnosis of human papillomavirus (HPV) at age 19. The patient's primary presenting symptoms included a 4-month history of severe painful menstrual cramps accompanied by painful intercourse. Severe menstrual cramping and pain began 4 months ago when oral contraceptives (OCs) were changed; the pain was so severe that she reported several instances of absence from work. Patient takes naproxen 550 mg daily when cramps and pain begin with no relief. Painful cramping starts 5–7 days before menses begin, with the worst pain experienced on the first day of flow; the pain disappears completely by the third day of flow. Ms. S is gravida 0; last normal menstrual period (LMP) began 6 days ago at her office visit. Her physical exam was unremarkable with the exception of a dry vaginal vault. She had been treated conservatively by her primary care physician with OCs and nonsteroidal anti-inflammatory drugs (NSAIDs) for her dysmenorrhea with no relief. Her surgical history included abdominal surgery as an infant to enclose the bladder inside the pelvic cavity with no subsequent problems. She also reported painful intercourse (dyspareunia) and vaginal dryness with penile thrusting for the past 4 months about 1 week before onset of her period. Patient reported an abnormal Papanicolau (Pap) smear 1 year prior to office visit. Patient requested human immunodeficiency virus (HIV) testing because she had never been previously tested. No history of sexually transmitted infections other than HPV. Patient reported no change in vaginal discharge with no itching, burning, or malodor. Patient reported having unprotected sexual intercourse with two partners during her lifetime.
Objective findings included Pap and pelvic annual exam with results of atypical squamous cells of undetermined significance (ASCUS)-HPV high-risk HPV in the previous year. Colposcopy at that time revealed no atypical cells. Pelvic exam performed 4 months earlier with negative Neisseria gonorrhoeae (GC) and chlamydia cultures.
- • Low-dose OC: 30 ethinyl estradiol/0.15 desogestrel one tablet by mouth (PO) every day.
- • Naproxen 550 mg daily as needed for menstrual pain.
This article presents a case study and comprehensive analysis with rationale of the potential differential diagnoses and care plan for the advanced practice registered nurse (APRN) in the primary care setting. Three of the most commonly presenting women's health-related conditions in a family-based practice include primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia. Although these conditions occur commonly, they can present a challenge in developing an accurate differential diagnosis and appropriate plan of care. A sample diagnostic and comprehensive treatment plan are also included.
The differential diagnoses for dysmenorrhea in a young, otherwise health female include primary and secondary dysmenorrhea, endometriosis, adenomyosis, pelvic inflammatory disease (PID), cervical stenosis, fibroids, ovarian cyst, and endometrial polyps. Each possibility will be considered below.
This diagnosis is likely in probability but the APRN must rule out pelvic pathology for definitive diagnosis. The differential diagnosis for primary dysmenorrhea or painful menstruation with no pathologic cause includes ruling out other conditions such as membranous dysmenorrhea and secondary or pathological dysmenorrhea caused by endometriosis, adenomyosis, PID, cervical stenosis, fibroids, ovarian cyst, and endometrial polyps (Decherney, Nathan, Goodwin, & Laufer, 2007; French, 2005). Primary dysmenorrhea is generally associated with ovulatory cycles with the mechanism of pain attributed to prostaglandin activity (Morrow & Naumberg, 2009). Generally, it is believed that ovulation becomes associated with menstrual cycles 2–4 years after menarche in most women, which is consistent with Ms. S's history (Zhang et al., 2008). Therefore, the diagnosis of primary dysmenorrhea is suggested by the onset of symptoms that coincide with the history of ovulation (Morrow & Naumberg). Primary dysmenorrhea generally does not occur at menarche, but generally occurs later in adolescence (Decherney et al. Morrow & Naumberg).
Ms. S's symptoms of menstrual cramping and pain did not begin until age 18, which is consistent with the outside window for the onset of primary dysmenorrhea. It is also important to note that “the prevalence of primary dysmenorrhea peaks in the second and third decades of life and decreases in frequency with advancing age as the prevalence of secondary dysmenorrhea increases” (Morrow & Naumberg, 2009, p. 19.) However, as many as 14%–26% of adolescents miss school or work as a result of primary dysmenorrhea pain (Decherney et al., 2007; French, 2005; Wolf & Schumann, 1999). Ms. S's symptoms of missing work and school on the first day of menses is also consistent with a diagnosis of primary dysmenorrhea. Primary dysmenorrhea pain generally occurs on the first day of menses when the menstrual flow begins, but it may not be present until the second day of flow (French; Morrow & Naumberg; Wolf & Schumann). In addition, nausea, vomiting, diarrhea, and headache may occur. In Ms. S's case, the symptoms of vomiting, diarrhea, or headache are missing. One distinction concerning primary dysmenorrhea is that symptoms associated with endometriosis (discussed below) are not present (Morrow & Naumberg). Ms. S's menstrual pain and cramping are somewhat consistent with primary dysmenorrhea, but she also has symptoms consistent with endometriosis, making a diagnosis of secondary dysmenorrhea a strong possibility.
Primary dysmenorrhea can be misdiagnosed as secondary dysmenorrhea because of endometriosis. However, the timing and onset of symptoms are helpful in differentiating primary and secondary dysmenorrhea (Decherney et al., 2007; Youngkin & Davis, 2004). Secondary dysmenorrhea because of endometriosis may cause pain that usually begins 1–2 weeks before menses with peak pain 1–2 days before menses that is relieved by the onset of menstrual flow (Decherney et al.; Morrow & Naumberg, 2009; Youngkin & Davis). In Ms. S's case, her symptoms are somewhat a mix of primary dysmenorrhea-related pain and secondary dysmenorrhea/endometriosis-related pain. Ms. S's menstrual cramping pain generally begins 5–7 days in advance of her period that is somewhat consistent with secondary dysmenorrhea from endometriosis. Endometriosis-related pain generally is relieved by the onset of flow (Decherney et al.). In contrast, Ms. S's menstrual pain is worse on her first day of flow, but does not subside until day 3 of her menstrual flow.
Another symptom Ms. S is experiencing that is unrelated to primary dysmenorrhea is dyspareunia. Dyspareunia that occurs with deep thrusting during intercourse is more often associated with endometriosis. Ms. S's dyspareunia that begins about 1 week before her period and ends with its onset is somewhat consistent with secondary dysmenorrhea/endometriosis. Because of Ms. S's age, onset of her symptoms, and mother's history of menstrual-related pain, it is likely that Ms. S has primary dysmenorrhea, but it is important to rule out other pelvic abnormalities such as endometriosis. Ms. S's pain is not relieved by her current dose of naproxen, another factor that could possibly indicate that her dysmenorrhea may not be related to primary dysmenorrhea prostaglandin activity. However, Ms. S. has been taking a substandard dose of naproxen 550 mg once daily. Before determining that naproxen is ineffective, a therapeutic trial at an accurate dose should be prescribed at 550 mg twice or even three times daily (Abramowicz & Zucotti, 2007).
In addition, Ms. S has not tried any different types of NSAIDs or antiprostaglandins other than naproxen to treat her pain. Ms. S only takes naproxen when she starts to experience pain. It is very possible that she will respond well to a therapeutic dose of naproxen or another NSAID such as ibuprofen (Abramowicz & Zucotti, 2007). Many women find one NSAID to be more effective than another, and tend to try various products before settling on a single effective medication and dosage (Morrow & Naumberg, 2009). In addition, taking NSAIDs consistently before the onset of pain has been shown to be effective with some patients (Dawood & Khan-Dawood, 2007). Some patients with primary dysmenorrhea do not get pain relief with medication. “It is estimated that as many as 10%–25% of women do not respond to NSAIDs or choose not to use them because of their related side effects” (Morrow & Naumberg, p. 24). However, a recent Cochrane Intervention Review found that NSAIDs provide effective relief for dysmenorrhea-related pain and appeared to be more effective than paracetamol. However, the comprehensive review of over seven databases did not demonstrate that any particular NSAID was safer or worked better than others (Marjoribanks, Proctor, Farquhar, & Derks, 2010). In addition, NSAIDs are known to cause adverse effects, including upset stomach, headache, and sleepiness (Abramowicz & Zucotti).
Another factor to consider is the fact that Ms. S's dysmenorrhea has not been relieved by taking OCs. In fact, she reported that her cramps have been “worse” since her prescription was changed from one she had taken for the past 18 months to an OC that has a slightly higher level of estrogen 4 months ago. OCs, particularly those with higher estrogen content, have been shown to prevent pain in most patients with primary dysmenorrhea who do not obtain relief with antiprostaglandins (Decherney et al., 2007). One Cochrane Review concluded that there is insufficient evidence from randomized control led trials to support the contention that low- and medium-dose estrogen OCs were effective in treating women with primary dysmenorrhea. In addition, this Cochrane Review demonstrated no difference between OC preparations (Wong, Farquhar, Roberts, & Proctor, 2009). Despite the lack of randomized control led trial data, nonsystematic reviews claim that OCs are up to 90% effective in the treatment of dysmenorrhea (Morrow & Naumberg, 2009; Smith, 2007). OCs prevent ovulation and alter endometrium formation that results in decreased prostaglandin activity and resultant pain. Because Ms. S has not experienced any pain relief by taking OCs, it is important to rule out other pelvic abnormalities.
This is likely in probability but the APRN must determine the source of pelvic pathology to make this diagnosis. The differential diagnosis for secondary dysmenorrhea includes endometriosis, adenomyosis, leiomyomas, intrauterine devices, PID, adhesions, cervical stenosis, ovarian cyst, and endometrial polyps. Each differential diagnosis will be analyzed for probability below.
Endometriosis This is likely in probability but cannot be confirmed without direct visualization of implants. Endometriosis should be considered in the differential diagnosis of virtually all pelvic disease because of its varied presentations. Endometriosis is the growth of cells similar to those that form the inside of the uterus (endometrial cells), but in a location outside of the uterus. Endometrial cells are the same cells that are shed each month during menstruation. The cells of endometriosis attach themselves to tissue outside the uterus and are called endometriosis implants (Milingos et al., 2006). The implants are most commonly found on the ovaries, the fallopian tubes, outer surfaces of the uterus or intestines, and on the surface lining of the pelvic cavity. Endometriosis should be considered in any patient of reproductive age complaining of pain or infertility (Decherney et al., 2007; French, 2005). Endometriosis is common among women of reproductive age and its clinical findings vary greatly depending upon the size, number, and extent of implants. Endometriosis is estimated to affect over 1 million women (estimates range from 3% to 18% of women) in the United States (French; Milingos et al.). Infertility, dysmenorrhea, and dyspareunia are the main presenting symptoms associated with endometriosis (Decherney et al.). Ms. S's concerns include dysmenorrhea and dyspareunia; however, she has never attempted to get pregnant, so her fertility is unknown. Endometriosis is likely in probability based only on Ms. S's history and timing of her symptoms but a definitive diagnosis cannot be made without further diagnostic testing (Decherney et al.; Milingos et al.).
Endometriosis is characterized by pain that begins 1–2 weeks before menses that reaches a peak 1–2 days before that is relieved at the onset of menstrual flow or shortly thereafter (Decherney et al., 2007). Ms. S reported cramping menstrual pain that begins 5 to 7 days before her period begins with excruciating pain on her first day of menses that disappears by the third day of her flow. Ms. S's symptoms are somewhat consistent with secondary dysmenorrhea from endometriosis; however, Ms. S's pain is not relieved by the onset of her flow. Instead, Ms. S's pain is at its worst on the first day of her menstrual flow that is consistent with a diagnosis of primary dysmenorrhea. Endometriosis is also characterized by pain during sexual intercourse or findings of adnexal tenderness or mass or cul-de-sac nodularity. Ms. S reported pain during sexual intercourse that begins about 1 week before her period begins and stops after her period begins, which is consistent with endometriosis-related pain. However, Ms. S's pelvic exam did not reveal any adnexal tenderness or cul-de-sac nodularity. Based on Ms. S's history and physical exam, it is likely that she has endometriosis but such a diagnosis cannot be confirmed and Ms. S's symptoms should first be treated to see if they resolve before considering invasive diagnostic procedures (Decherney et al.; Milingos et al., 2006).
Adenomyosis This is unlikely in probability. Adenomyosis is a condition where the tissue that lines the uterus (endometrium) grows within the uterus’ muscular outer walls. Adenomyosis generally occurs in women late in their childbearing years after they have born children (Decherney et al., 2007; V. L. Katz, 2007). Adenomyosis is characterized by excessive menstrual bleeding that is heavy or prolonged, severe cramping or sharp, knife-like pain during menstruation, dysmenorrhea that lasts throughout a woman's period worsens with age, painful intercourse, menorrhagia, passing blood clots during menstrual period, and a uterus that is symmetrically double or triple normal size (Decherney et al.; V. L. Katz). In this case, Ms. S is only 22 years of age, making a diagnosis of adenomyosis unlikely. In addition, her uterus was small in size upon physical exam. Although Ms. S has dyspareunia and dysmenorrhea, she is not experiencing any other symptoms associated with adenomyosis. Therefore, a diagnosis of adenomyosis is unlikely.
Leiomyomas Possible, but not likely in probability. Uterine leiomyomas are benign tumors composed of smooth muscle and fibrous connective tissue. They are also referred to as fibromyomas, fibromas, fibroleiomyomas, fibroids, or simply myomas (Hildreth, Cassio, & Glass, 2009; Van Voorhis, 2009). They can occur singly but often are multiple, with variations in size. In addition, leiomyomas are more common in African-American than in white women (Hildreth et al.). The etiology of leiomyomas is not fully understood, but it is suspected that they are monoclonal tumors resulting from somatic mutations of one single neoplastic cell. It is also thought that estrogens, progesterone, and human growth hormone play an important role in the regulation of the tumor growth (Hildreth et al.; Van Voorhis). Symptoms occur only in 35%–50% of affected patients, with the number one symptom reported being abnormal, excessive uterine bleeding or menorrhagia. Leiomyomas may also cause acute pain that may be characterized as dysmenorrhea or dyspareunia. Other symptoms include urinary frequency, urinary retention, ureteral obstruction, and hydronephrosis (Hildreth et al.; Van Voorhis). In this case, while Ms. S's periods have been slightly heavier for the past 4 months, they are not excessively heavy. In addition, Ms. S's pain is only acute for the first day of her menses and she is not experiencing any urinary symptoms. Ms. S's dyspareunia is only experienced for about 1 week before her period and disappears after her period begins. Based on Ms. S's history and physical exam, a diagnosis of leiomyomas is possible but not likely.
PID/infection Possible but not likely in probability. PID infection and inflammation develop in the pelvic organs, including the uterus, fallopian tubes, and ovaries. PID is a general term for acute, subacute, recurrent, or chronic infection of the oviducts, ovaries, and adjacent tissues. Most PID infections result from the bacterial agents N. gonorrhoeae (GC) and Chlamydia trachomatis, but they can even be viral or parasitic (Decherney et al., 2007). Mycoplasma genitalium can also be an important and frequent cause of female lower genital tract infections. It is important to note that infections with M. genitalium and C. trachomatis are often asymptomatic, with no significant differences between the bacteria in terms of symptoms (Falk, Fredlund, & Jensen, 2005). In this case, PID is possible, but not likely considering all differential diagnoses because Ms. S has no prior history of PID, no previous sexually transmitted infections (STIs) other than HPV, and no change in her vaginal discharge. However, PID must always be considered because it frequently presents with bilateral/diffuse lower abdominal or pelvic pain.
Ms. S does not have any fever, nausea, or vomiting. PID is generally characterized by the onset of lower abdominal and pelvic pain, vaginal discharge, abdominal, uterine, adnexal, and cervical motion tenderness in addition to one or more of the following: temperature above 101°F, leukocyte count greater than 10,0000, gram-negative intracellular diplococci in cervical secretions, purulent material, and an elevated erythrocyte sedimentation rate (Decherney et al., 2007). Ms. S. has none of the symptoms generally associated with PID. Diagnosis of PID is generally confirmed by adnexal tenderness and chandelier sign, neither of which was found on examination. In addition, Ms. S does not have bilateral or diffuse pelvic pain. Ms. S's negative STI tests for N. gonorrhoeae and C. trachomatis 4 months ago in addition to her history of a monogamous sexual relationship for the past 2 years also decreases the likelihood of a diagnosis of PID.
Adhesions Possible but only somewhat likely in probability. An adhesion is a band of scar tissue that binds two parts of tissue together that should remain separate. Adhesions develop when the body's repair mechanisms respond to any tissue disturbance, such as surgery, infection, trauma, or radiation. Abdominal adhesions are a common complication of surgery, occurring in up to 93% of people who undergo abdominal or pelvic surgery so they should always be considered in a postsurgical patient. However, abdominal adhesions also occur in 10.4% of people who have never had surgery (Hammoud, Gago, & Diamond, 2004). Ms. S's surgery occurred when she was an infant, and her pain did not begin until nearly 18 years later. Adhesions typically begin to form within the first few days after surgery, but they may not produce symptoms for months or even years (Hammoud et al.). Pain with intercourse caused by pelvic adhesions is a potential sign of pelvic adhesions. In addition, endometriosis can cause adhesions that cause tissues and organs to become stuck together. Pain from adhesions can be relieved by removing the adhesions through laparoscopic resection, ablation, or surgery. Most commonly, adhesions cause pain by pulling nerves, either within an organ tied down by an adhesion or within the adhesion itself (Hammoud et al.). Because Ms. S's dyspareunia is periodic in nature and occurs only a week before her period and ceases with menstrual flow, abdominal adhesions are possible, but not a likely cause of her pain.
Cervical stenosis This is unlikely in probability. Cervical stenosis is a narrowing of the cervical opening. Cervical stenosis can lead to obstruction of menstrual flow and dysmenorrhea in premenopausal women. Cervical stenosis may be congenital, inflammatory, neoplastic, or surgical in origin and may be partially or completely occlusive. Many cases of cervical stenosis follow surgical manipulation of the cervix (Decherney et al., 2007; Youngkin & Davis, 2004). In Ms. S's case, she has not experienced any change in her menstrual flow other than it has been slightly heavier for the past 4 months. Her periods have not changed in their duration and her cervix was pink with a small round os upon physical examination. The swab and brush were inserted with ease to obtain specimens. Ms. S has never had any cervical surgeries, ablations, cervical or uterine cancer, or radiation therapy frequently associated with cervical stenosis. Based upon her history and physical exam, cervical stenosis is an unlikely cause of Ms. S's dysmenorrhea.
Ovarian cyst Unlikely in probability. Ovarian enlargement by a benign mass or cyst can cause twisting of the ovary and tube to cause acute, severe abdominal pain that may be accompanied by nausea and vomiting. Ms. S has no nausea, vomiting, or severe abdominal pain. Most significantly, her abdomen was soft, and nontender with no adenexal tenderness; the ovaries were smooth and almond like in size upon palpation without adenexal tenderness. However, ovarian cysts should be considered because they can cause pain if they twist the ovary causing intermittent pain (Tierney, McPhee, & Papadakis, 2007). Ms. S's pain is related to the onset of her menses and subsides by the third day of her menstrual flow. In addition, Ms. S has been on OCs for the past 2 years and has taken them continuously, which reduce her chances of experiencing an ovarian cyst. Ms. S has no history of menstrual irregularities with menstrual cycles that occur at 28-day intervals. Ovarian cysts often present with menstrual irregularities (Decherney et al., 2007; Youngkin & Davis, 2004). Ms. S's history is not consistent with an ovarian cyst, making it unlikely in probability.
Endometrial polyps This is very unlikely in probability. Endometrial polyps consist of areas in the uterus where the lining (endometrium) becomes overgrown and forms a mass (polyp). Uterine polyps may attach to the interior of the uterus by a large base or a thin stalk and range in size from a few millimeters to several centimeters. Although endometrial polyps can happen at any time, uterine polyps most commonly occur in women in their 40s and 50s. Many women with uterine polyps are asymptomatic, but generally, these women experience one or more of the following: irregular menstrual bleeding, such as bleeding varying amounts at frequent but unpredictable intervals, bleeding between menstrual periods, excessively heavy menstrual periods (Decherney et al., 2007; Dreisler, Sorensen, Ibsen, & Lose, 2009). In Ms. S's case, her age makes her an unlikely candidate for endometrial polyps. In addition, she does not have irregular menstrual bleeding, bleeding between periods, or excessive flow. Based upon Ms. S's history, a diagnosis of endometrial polyps is very unlikely.
Membranous dysmenorrhea Highly unlikely in probability. The diagnosis of membranous dysmenorrhea includes primary dysmenorrhea and secondary dysmenorrhea. Membranous dysmenorrhea is rare; it causes intense cramping pain because of passage or shedding of a cast of the endometrium as a single entity through an undilated cervix (Decherney et al., 2007). In Ms. S's case, there have been no changes in her menstrual flow. Ms. S reported no clotting or tissue in her menstrual flow that might indicate membranous dysmenorrhea. In Ms. S's case, a diagnosis of membranous dysmenorrhea should be considered a “zebra” among the “horses” of more commonly occurring differential diagnoses making it highly unlikely.
Dyspareunia secondary to inadequate lubrication
This is very likely in probability. Inadequate lubrication remains one of the primary causes of dyspareunia (DeCherney et al., 2007). The vagina produces lubrication during sexual arousal, but many women experience inadequate lubrication related to low estrogen states such as postpartum and menopausal stages, lack of sexual arousal or foreplay, and certain medications that inhibit arousal and production of lubrication (DeCherney et al.). Although a drop in estrogen can occur at any age, Ms. S's inadequate lubrication is unlikely to be associated with a low estrogen state. She is 20 years old, not postpartum, has regular periods, and is not menopausal with no decreased vaginal elasticity associated with aging. While the two medications that Ms. S is taking at their current doses are not generally associated with inadequate lubrication, Ms. S's complaints of vaginal dryness for the past 4 months in addition to her pelvic exam that revealed a dry vaginal vault supports a diagnosis of dyspareunia secondary to inadequate lubrication. Based on Ms. S's history, a diagnosis of dyspareunia secondary to inadequate lubrication is very likely in probability.
Dyspareunia secondary to endometriosis Likely in probability but cannot be confirmed. The differential diagnosis for dyspareunia includes inadequate lubrication, low estrogen states such as postpartum and menopausal stages, intact hymen, tender episiotomy scar, decreased elasticity associated with aging, Bartholin's gland abscess or lesions, clitoral irritation, clitoral infection, vaginal infections, sensitivity reactions, atrophic reactions, endometriosis, PID, and ectopic pregnancy (Decherney et al., 2007). Ms. S has been sexually active for several years and does not have an intact hymen. She had no lesions, abscesses, lesions, clitoral irritation, or infection upon physical exam, nor has she used any new soaps or products that might be associated with a sensitivity reaction. Ms. S's dyspareunia could be caused by PID, but her history and symptoms make a diagnosis of PID unlikely. Ms. S's LMP was approximately 6 days ago, making an ectopic pregnancy highly unlikely; however, the symptoms of pain upon deep penetration by her partner are consistent with endometriosis. In addition, Ms. S's pain begins approximately 1 week before her period when her potential endometrial implants would be enlarged and disappears when her flow begins. Ms. S's history and symptoms are consistent with dyspareunia caused by lack of lubrication or endometriosis.
- 1Primary dysmenorrhea—If, after ruling out all other pathological causes for dysmenorrhea and without a definitive diagnosis of endometriosis, primary dysmenorrhea would be the likely diagnosis for Ms. S. given the normal pelvic exam. The presence of menstrual pain that is most acute on the first day of menses and is not relieved by the onset of flow, plus a history of maternal menstrual pain supports a diagnosis of primary dysmenorrhea (Decherney et al., 2007).
- 2Secondary dysmenorrhea because of endometriosis—Cannot make a definitive diagnosis without direct visualization of endometrial implants; however, based on Ms. S's symptoms this diagnosis remains likely in probability (Decherney et al., 2007; Youngkin & Davis, 2004). The presence of premenstrual cramping pain for 5–7 days coupled with dyspareunia that occurs with deep penile thrusting 1 week before menses and disappears upon menses supports a diagnosis of secondary dysmenorrhea due to endometriosis.
- 3Dyspareunia secondary to inadequate lubrication—Inadequate lubrication is one of the primary causes of dyspareunia (Decherney et al., 2007). Ms. S's complaints of vaginal dryness in addition to her pelvic exam that revealed a dry vaginal vault supports a diagnosis of dyspareunia secondary to inadequate lubrication.
- 4Dyspareunia secondary to endometriosis—Ms. S's concerns of dyspareunia with deep penile thrusting that occurs 1 week before menses and is relieved by the onset of menses are consistent with dyspareunia secondary to endometriosis. However, further diagnostic testing including laparoscopy or laparotomy because of previous pelvic surgery is required for a confirmatory diagnosis (Decherney et al., 2007; Youngkin & Davis, 2004).
- 5At Risk for cervical dysplasia because of previous HPV infection—HPV lab results pending. Ms. S's history of HPV infection as indicated by her ASCUS high-risk Pap smear 1 year ago places her at risk for cervical dysplasia. Although Ms. S's colposcopy revealed no cervical dysplasia and pending the results of Ms. S's HPV test results, Ms. S continues to be at risk for cervical dysplasia.
- 6At risk for HIV because of unprotected sex—HIV labs pending. Any sexually active person that is having unprotected sex and not using condoms is at risk for contracting HIV. Ms. S has had two sexual partners, one of whom infected her with HPV. She is not aware of how many sexual partners that her first partner had or if he practiced safe sex by wearing condoms. Ms. S's sexual history places her at risk for HIV.
- 7At risk for GC and chlamydia—GC and chlamydia cultures pending. Although Ms. S's history places her at very low risk of GC and chlamydia, she is a sexually active collegiate who does not practice safe sex and this places her at risk for contracting all STIs including GC and chlamydia.
- 1Refer to specialist for laparoscopy or laparotomy after 4–6 months of the therapeutic regimen (discussed below) if no relief from dysmenorrhea or dyspareunia is obtained to determine the presence of endometrial implants or other pathological causes for pain, including pelvic adhesions. Because of Ms. S's previous abdominal surgery, laparoscopy may not be feasible even though it is less invasive than a laparotomy. Ms. S's menstrual pain is debilitating and is affecting her daily life. If her symptoms are not improved by the therapies implemented below, further diagnostic testing is recommended. The use of other ancillary diagnostic studies such as ultrasound, x-ray, and computed tomographic scans are of little use in diagnosing endometriosis. CA-125 (cancer antigen) is cost effective and is often elevated in women with endometriosis, but it can be elevated by many other pelvic diseases and is not specific to endometriosis (Decherney et al., 2007). The reference standard test for diagnosis and staging of endometriosis is laparoscopy or laparotomy with biopsy. It should be considered when first-line therapies are ineffective and dysmenorrhea causes functional impairment (French, 2005). In addition, laparoscopy or laparotomy will allow for treatment by ablation or removal of any endometrial implants or adhesions or other pathologies if present.
- 2In adolescents such as Ms. S who are 20 years of age or younger, low-grade squamous intraepithelial lesions (LSIL) or ASCUS detected by screening should be monitored with repeated cytology every 12 months. If high-grade squamous intraepithelial lesions (HSIL) or atypical squamous cells, cannot exclude HSIL (ASC-H) is detected, Ms. S should be referred to colposcopy for biopsy. If, at this first 12-month follow-up the cytology is normal or if LSIL or ASCUS is detected, continued monitoring is recommended. Routine screening should resume if cytology is normal at the second 12-month follow-up (at 24 months). If cytology shows LSIL, ASCUS, ASC-H, or HSIL, referral for colposcopy is warranted (American Society for Colposcopy and Cervical Pathology [ASCCP], 2007; Brismar, Johansson, Borjesson, Arbyn, & Andersson, 2009; Moscicki, 2008; Widdice & Mosciki, 2008).
Primary dysmenorrhea or secondary dysmenorrhea/endometriosis Treat empirically with hormonal therapy/OC to delay Ms. S's periods.
Regardless if Ms. S's dysmenorrhea is primary or secondary to endometriosis, treatment with OCs is recommended to delay her periods and therefore limit her dysmenorrhea symptoms related to menstruation. There are several OC options to delay her periods and limit her dysmenorrhea related to menstrual flow. Any monophasic OC containing 20–35 micrograms of estrogen (ethinyl estradiol) can be used to delay a woman's menstrual cycle. OCs prevent ovulation and reduce prostaglandin production if Ms. S's dysmenorrhea is truly primary in nature. In addition, monophasic OCs disrupt or interrupt the cycles of stimulation and bleeding of endometriotic tissue if her dysmenorrhea is secondary to endometriosis (Lehne, 2007). The continuous exposure to combination OCs can result in decidual changes in the endometrial glands and has been shown to be effective in decreasing dysmenorrhea and even retarding the progression of endometriosis (Decherney et al., 2007). If a generic monophasic pill is prescribed, Ms. S. should take active pills from two pill packs for 6 weeks in a row and then take inactive pills during week 7. If she experiences no unpredictable bleeding or side effects during this cycle, she would then take active pills for 9 weeks consecutively in the next cycle and 12 weeks in the following cycle to eventually limit her periods to four times yearly. Using generic OCs may provide the most cost-effective method for limiting Ms. S's periods, but this requires the patient to use multiple pill packs and discard inactive pills.
Another option currently on the market is the OC Seasonale, a 91-day extended-cycle pack containing 84 consecutive active then 7 inert tablets that are started on day 1 of the menstrual cycle or on first Sunday after onset of menses. Seasonale contains 0.03 ethinyl estradiol with 0.15 levonorgestrel (Lehne, 2007). Because Seasonale provides 84 consecutive days of active pills, it will limit Ms. S to having approximately four (4) periods per year instead of twelve (12) to reduce the number of first menstrual flow days, when Ms. S is most acutely affected. Prepackaged extended pill packs provide a convenient method for patients to keep track of their pills and do not require discarding inactive pills. However, such prepackaged pill packs may cost more depending upon individual insurance coverage.
A third option is the OC Seasonique, which provides a pill pack with 84 days of pills containing ethinyl estradiol/levonorgestrel (0.03/0.15) followed by 7 days of pills containing ethinyl estradiol at (0.01/0), a very low dose of estrogen. The use of low-dose estrogen pills instead of inactive pills during week 13 could limit uncomfortable symptoms associated with a hormone-free interval such as lighter periods and less bloating (Epocrates, 2009). Another option available that could delay Ms. S's periods for up to 12 months is Lybrel. Lybrel is a low-dose extended-use contraceptive that contains low doses of progesterone and estrogen (Tarascon Pocket Pharmacopoeia, 2007). Lybrel is designed to be taken daily for a period of 12 months with no hormone-free intervals and no periods for 1 year. Approximately 50% of women that take lybrel experience no periods at the end of one year's treatment. Approximately, 4 of 10 women experience spotting or bleeding that requires wearing protective pads (Epocrates). Each of these treatment options should be discussed with Ms. S so that she can choose the option that is best for her.
Naproxen 550 mg PO should be taken with food twice daily or three times daily beginning 3 days before the end of active pill pack and discontinued when cramping subsides after menses.
Because Ms. S took a substandard dose of naproxen with no relief in the past, a trial of naproxen prescribed at the appropriate therapeutic dose should first be used to determine if pain relief can be obtained. Naproxen 550 mg taken twice daily or even three times daily for the management of more severe pain has been shown to be effective in the treatment of dysmenorrhea. “The mainstay of pharmacologic treatment of primary dysmenorrhea spans across the several classes of prostaglandin synthetase inhibitors, including aspirins, fenamates, and nonsteroidal anti-inflammatory medications (NSAIDs)” (Morrow & Naumberg, 2009, p. 24). Prostaglandin inhibitors such as naproxen have been shown to decrease the intensity of symptoms associated with high levels of endometrial prostaglandins. “Their effectiveness results from cyclooxygenase inhibition and a subsequent decrease in prostaglandin production, leading to diminished concentration of prostaglandins in endometrial fluid and decreased uterine tone” (Morrow & Naumberg, p. 24). Approximately 70% of women experience moderate to complete relief of dysmenorrhea-related symptoms with the use of prostaglandin inhibitors prescribed and taken at appropriate dosages; however, individual trials show wide variations in range (Morrow & Naumberg; Owen, 2004).
Analgesic alternative therapy
Ibuprofen 400 mg PO can be taken with food every 4–6 hours beginning 3 days before end of active pill pack and discontinued when cramping subsides after menses.
If Ms. S achieves no relief with a therapeutic dose of naproxen, changing her to a different NSAID such as ibuprofen may be effective in relieving her menstrual discomfort. Ibuprofen is an NSAID/antiprostaglandin that works by blocking prostaglandin synthesis and metabolism. Antiprostaglandins such as ibuprofen must be taken before pain is established because they are much less effective after the onset of pain (Decherney et al., 2007). In addition, Ms. S states that her mother's menstrual cramps are relieved by ibuprofen. Utilizing a patient-centered approach to care, if Ms. S is more comfortable taking a medication that effectively manages dysmenorrhea for her mother, then such a choice is reasonable in selecting equivalent treatment options. Ibuprofen is an NSAID that is available over the counter that has been extremely effective in reducing menstrual prostaglandin and relieving dysmenorrhea (Decherney et al.). Ibuprofen is also fairly inexpensive. Ibuprofen should be tried and evaluated for relief before potentially changing to a prescription type medication such as celecoxib (Celebrex), a COX-2 inhibitor, or stronger analgesic such as codeine (Daniels, Gitton, Wenchun, Stricker, & Barton, 2008). In addition, NSAIDs such as ibuprofen are appropriate sole therapy for women with mild menstrual pain associated with minimal endometriosis (Abramowicz & Zucotti, 2007). Because Ms. S has severe dysmenorrhea, adding NSAID therapy plus OCs will work synergistically to improve dysmenorrhea (Decherney et al.).
The application of low-level topical heat therapy has been shown to be as effective as ibuprofen in treating dysmenorrhea. However, the practicality of applying continuous low-level heat during the activities of daily living such as attending class and working may be somewhat impractical (Akin et al., 2001; Decherney et al., 2007; Morrow & Naumberg, 2009).
Diets low in fat and meat products have been shown to decrease serum sex-binding globulin and decrease the duration and intensity of dysmenorrhea (Decherney et al., 2007; Morrow & Naumberg, 2009). Low-fat vegetarian diets have been associated with increased serum sex hormone binding globulin concentration and reductions in body weight, dysmenorrhea duration and intensity, and premenstrual symptom duration. The decreased dysmenorrheal symptom effects might be mediated by dietary influences on estrogen activity (Barnard, Sciallie, Hurlock, & Bertron, 2000).
Dyspareunia secondary to inadequate lubrication
The application of personal lubricants can decrease dyspareunia by decreasing the friction of penile entry. Because Ms. S reported experiencing vaginal dryness for the past 4 months at the onset of her painful intercourse, application of a personal lubricant to the vaginal opening may decrease the dyspareunia that Ms. S is experiencing (A. Katz, 2007). In addition, taking sufficient time for foreplay before sex allows time for a woman's body to produce natural lubricants that can facilitate penile entry and reduce friction (Goldstein, Pukall, & Goldstein, 2009).
Dyspareunia secondary to endometriosis
Changing sexual positions can alleviate dyspareunia for many individuals that experience pain during intercourse. Ms. S indicated that she and her partner were willing to try different positions to relieve discomfort. If a woman utilizes the top position, she has more control over the depth of penetration and may decrease dyspareunia (Goldstein et al., 2009).
At risk for cervical dysplasia because of previous HPV infection
Gardasil vaccine protects against the four major strains of HPV that cause the majority of cervical cancers and genital warts (Herrero, 2009). In uninfected women, Gardasil can cause a 70% reduction in cervical cancers and a 90% reduction in genital warts. In Ms. S's case, even though she has had an HPV infection, she may still get some benefit from the vaccine because we do not know to which specific strains of virus she was previously exposed. For example, if Ms. S was not exposed to HPV 16 that is associated with over 50% of cervical cancers, she would still benefit from taking Gardasil (Herrero). Ideally females should receive vaccination for HPV before they become sexually active. In this case, Ms. S is sexually active and has been previously diagnosed with HPV. Therefore, it would be extremely important to explain to her that she would receive less benefit from taking the vaccine because she has previously been diagnosed with HPV and may have already contracted an HPV type targeted by the vaccine. However, few sexually active young women are infected with all HPV types covered by the vaccine, so Ms. S could still get protection against the types she has not contracted (Centers for Disease Control and Prevention [CDC], 2009). The 2008 updates on Gardasil from the Advisory Committee on Immunization Practices (ACIP) demonstrate efficacy was seen in the subset of 16- to 26-year-old women who were polymerase chain reaction (PCR)-negative and seropositive at baseline. However, no efficacy (positive or negative) was seen in the subset of women PCR positive and seropositive at baseline (Haupt, 2008). The related costs and potential benefits of the Gardasil series should be explained in detail to Ms. S so that she can make an informed decision related to efficacy and cost.
- 1Review GC and chlamydia results with patient.
- 2After going over results with patient and answering any of her questions, treat for any GC or chlamydia infection if detected.
- 3If positive for GC, explain to patient that all sexual contacts must be notified and treated. Answer any questions and address any concerns that the patient might have.
- 4Rescreen for C. trachomatis and GC 4–6 weeks after completion of therapy if GC and/or chlamydia cultures come back positive (Uphold & Graham, 2003).
- 5Schedule appointment to go over HIV test results.
- 6Schedule appropriate counseling/referrals, additional testing, and treatment if HIV results are positive.
- 7Go over HPV test results with patient in 1 week. Answer any questions and address any patient concerns at that time.
- 9If HPV results are negative, re-check after first period on selected OC regime to evaluate the effectiveness of treatment regimen in alleviating menstrual pain and dyspareunia.
- 10Provide Gardasil immunization series upon patient's decision at 0-, 2-, and 6-month intervals.
- 11If no relief is obtained from treatment regimen, explore other pain control options and discuss referral to specialist for further diagnostic testing.
In conclusion, three of the most commonly presenting women's health-related conditions in a family-based practice include primary dysmenorrhea, secondary dysmenorrhea, and dyspareunia. Although these conditions occur commonly, the development of a comprehensive plan of care and accurate differential diagnoses remains an interesting challenge for the APRN.
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