Dysfunctional Uterine Bleeding in Adolescents
Dysfunctional Uterine Bleeding in Adolescents
Authors: Roytesa R. Savage, MD, FAAP, Assistant Professor of Pediatrics, Brody School of Medicine, Greenville, North Carolina; Shevonda Sherrow, MD, Assistant Clinical Professor, Department of Obstetrics and Gynecology, The Brody School of Medicine, Greenville, North Carolina.
Peer Reviewer: John Santamaria MD, FAAP, FACEP, Affiliate Professor of Pediatrics, University of South Florida School of Medicine, Tampa, Florida.
It is very common for adolescent females to present with menstrual irregularities and differentiating normal variations from life-threatening problems is critical to the emergency department physician. Unfortunately, dysfunctional uterine bleeding is a diagnosis of exclusion and should only be used when pathologic disease processes, such as ectopic pregnancy, coagulopathies, abuse, and foreign body have been excluded. Once more serious diseases have been excluded, the treatment is based on hemodynamic stability and degree of anemia. The authors review the physiology, unique aspects of menstruation in the adolescent, differential diagnosis, and treatment options for an adolescent with dysfunctional uterine bleeding.
— The Editor
Introduction
The onset of menstruation, menarche, is one of the last physiological changes of puberty but has a great emotional impact for an adolescent. Menstruation is associated with a lot of variation, causing anxiety for patients as well as parents. Only 2% of teens in one study recalled receiving information from their health care professional about menstruation.1 Therefore, emergency medicine physicians frequently are confronted with patients with menstrual irregularities and must differentiate more serious life-threatening diseases from common normal variations in menstruation. A common issue for adolescents is dysfunctional uterine bleeding. Dysfunctional uterine bleeding is the diagnosis used when there is no other pathology found for irregular or prolonged bleeding. The most common abnormality found in adolescents is anovulatory bleeding, which is characterized by an immature hypothalamic-pituitary-ovarian axis. Nonetheless, there must be a complete history and physical exam and appropriate diagnostic testing to rule out life-threatening disorders before the diagnosis of dysfunctional uterine bleeding is assigned to a patient. To further understand dysfunctional uterine bleeding, fundamental concepts of normal menstrual development, terminology, and presentations must be completely understood.
Physiology
The menstrual cycle can be separated into the follicular and the luteal phases. The two phases have distinct beginning and ending points that are regulated by various hormones. Variation exists in each menstrual cycle length, but the most common is a 28-day cycle. The follicular phase, proliferative phase, begins with sloughing of the endometrium on day 1 and ends with ovulation. The luteal phase begins with ovulation on approximately day 14 and ends with menstruation on day 28.
The follicular phase is marked with the release of gonadotropin-releasing hormone from the hypothalamus. The hypothalamus signals the anterior pituitary gland to produce and release follicle stimulating hormone (FSH) and luteinizing hormone (LH). The FSH stimulates the ovarian follicles to mature and they release estrogen. Estrogen serves several roles in the menstrual cycle. As the estrogen level increases, it causes proliferation of the endometrium. Moreover, estrogen elevations produce negative feedback to the pituitary, which in turn signals FSH to decline and stimulates the increase in LH.
This stimulation in the LH marks the beginning of the luteal phase. The increasing secretion of LH stimulates ovulation of the oocyte from the dominant follicle. The formation of the cyst after ovulation induces the maturation of the theca and granulosa cells to create a corpus luteum. The remaining cast becomes the corpus luteum, which is endocrinely active by producing progesterone in order to support an embryo or early pregnancy.2-8 The progesterone proceeds to provide a negative feedback on the production of LH, FSH, and gonadotropin-releasing hormone and stabilizes the endometrium by stopping proliferation. In preparation for potential implantation, the endometrium has increased vascularity. If no pregnancy occurs, the corpus luteum involutes, causing progesterone and estrogen levels to fall. The endometrium then sloughs away and menses begins. Since the levels of estrogen and progesterone are decreasing, their negative feedback on the hypothalamus and pituitary are removed and the process begins anew.2-9,10,11
Pathophysiology
There is great contrast between adolescent and adult menstrual cycles. The average age of menarche in the United States is 12.4 years with a range of 9–16 years.2,5,12 Maturation of the hypothalamic-pituitary-ovarian axis takes an average of two years but may take up to five years. To compound the issue, adolescents have a decreased amount of estrogen, LH, FSH, and progesterone compared with adult levels. There is continuous secretion of estrogen at lower levels with no feedback to the hypothalamus and pituitary to stimulate the production and release of an oocyte; hence, no corpus luteum and progesterone. Without ovulation, a corpus luteum is not produced and there are no increasing progesterone levels. If there is no increase in the progesterone levels, there is no progesterone-induced desquamation and bleeding. The endometrium can be unstable in light of the unopposed estrogen, with fragility of the endometrium and its vessels. There is little stromal (connective tissue) support provided without the progesterone effects on the endometrium. Without the support of progesterone, the endometrial growth is not stabilized. The spiral arterioles are noted to be more edematous and torturous as they continue to be exposed to the unopposed estrogen. Once the endometrial lining finally collapses with the thickened endometrium from the unopposed estrogen, the menses can be heavy and persist for a prolonged period of time.2-9,13-15
Lack of adequate progesterone production can cause local chemical derangements in the endometrium. Studies show that prostaglandin plays a major role in regulation of uterine bleeding. PGE2 produced vasodilatation and PGF2α increases vasoconstriction, while thromboxane promotes platelet aggregation and prostacyclines inhibit this process. In normal ovulatory cycles the ratio of PGF2α to PGE2 increases toward menses; whereas, there is a decreased ratio in anovulatory cycles. There is a decreased production of PGF2α without progesterone; however, PGE2 remains the same. In summary, the normal physiology of desquamation by vasoconstriction is reduced and vasodilatation is enhanced leading to increased uterine bleeding.3,10,16,17
Definitions
The normal menstrual cycle during adolescence can be 21 to 45 days in length during the first three years after menarche. This time shortens as the HPO axis matures to 21 to 35 days. The length of flow of menses in adolescents is an average of four days of bleeding, but can range from two to eight days. The average blood loss during the menstrual cycle is approximately 30 mL, with 80 mL as the upper limits.18-20
In defining dysfunctional uterine bleeding, all of the definitions of bleeding irregularities must be reviewed. (See Table 1.) Dysfunctional uterine bleeding is irregular and/or prolonged vaginal bleeding or abnormal vaginal bleeding due to unorganized endometrial sloughing in the absence of structural pathology or any other identifiable pathological cause. Menorrhagia is prolonged or heavy uterine bleeding that occurs at regular intervals. Metrorrhagia is uterine bleeding that occurs at irregular intervals. Menometrorrhagia is prolonged or heavy uterine bleeding that occurs at irregular intervals. Oligomenorrhea is uterine bleeding that occurs at prolonged intervals of 41 days to three months but is normal in flow, duration, and quantity. Polymenorrhea is uterine bleeding that occurs at an increased frequency of 21 days or less. Secondary amenorrhea is defined as no bleeding for six months after having uterine bleeding. Intermenstrual bleeding or spotting is uterine bleeding of variable amounts occurring between regular menstrual periods.20
Table 1. Terminology of Abnormal Uterine Bleeding |
Acute emergent abnormal uterine bleeding: leeding is characterized by significant blood loss that results in hypovolemia or shock Dysfunctional uterine bleeding: Ovulatory or anovulatory bleeding diagnosed after the exclusion of pregnancy or pregnancy-related disorders, medications, iatrogenic causes, obvious genital pathology and systemic conditions Menorrhagia: Prolonged or heavy uterine bleeding that occurs at regular intervals Metrorrhagia: Uterine bleeding that occurs at irregular intervals Menometrorrhagia: Prolonged or heavy uterine bleeding that occurs at irregular intervals Oligomenorrhea: Uterine bleeding that occurs at prolonged intervals of 41 days to 3 months but is normal flow, duration, and quantity Polymenorrhea: Uterine bleeding that occurs at an increased frequency of 21 days or less Primary amenorrhea: Absence of any spontaneous menses in an individual older than 16.5 years of age Secondary amenorrhea: Absence of menses for 6 months or the length of time equal to previous cycles after having uterine bleeding |
Epidemiology
In more than 90% of adolescents who have abnormal uterine bleeding, dysfunctional uterine bleeding caused by anovulation is usually the diagnosis. Thus, fewer than 10% of cases of abnormal bleeding have a structural, endocrine, iatrogenic, or clotting cause. However, if an adolescent is admitted to the hospital the incidence of identifiable diagnosis increases to 25%. Coagulation disorders occur in approximately 20% of adolescent females who are hospitalized.21-25
Differential Diagnosis
The unique aspect of dysfunctional uterine bleeding is that it is a diagnosis of exclusion. Therefore, by reviewing the differential diagnosis, other pathology must be excluded. There are many possible etiologies of abnormal uterine bleeding; therefore, an organized algorithm is essential. The "A, B, C, Ds" of abnormal bleeding in the adolescent are described in Table 2.
Table 2. 'ABCDs' of Abnormal Uterine Bleeding |
Abuse/Accidents/Foreign Objects. Abuse, accidents, and foreign objects may all result in abnormal vaginal bleeding. Abuse should be suspected when the demeanor of the child is unusual or the history does not correlate with the physical exam. The physical exam of the abused adolescent sometimes reveals a torn hymen at 5 o'clock and 7 o'clock, and sexually transmitted infections may coexist.
Accidents in adolescent girls are common.26-28 The most common are straddle injuries, which have a distinct appearance, characterized with vulvar edema and swelling with possible clitoral lacerations. Lastly, foreign objects such as crayons and small toys in the vaginal vault can cause vaginal bleeding secondary to local irritation and infection.
Iatrogenic Etiologies. Iatrogenic causes of abnormal uterine bleeding should be considered and include commonly used medications such as anticoagulants, selective serotonin reuptake inhibitors, antipsychotics, corticosteroids, hormonal medications, and tamoxifen. Herbal medications have also been implicated and include ginseng, ginkgo, and soy supplements that may alter estrogen levels or clotting parameters.29
Trauma. Vaginal lacerations must be ruled out as the cause of bleeding. Vaginal lacerations can be very severe and lead to blood transfusions. If not identified and treated as uterine bleeding, vaginal lacerations yield high morbidity. Vaginal trauma is not always due to abuse. Approximately 80% of vaginal lacerations are due to poor vaginal lubrication and sexual instrumentation. The most common is a transverse tear of the posterior fornix. Other common areas of trauma are linear tears of the right or left vaginal fornices.16
Hypothalamic-Pituitary-Ovarian Axis. The most common cause of dysfunctional uterine bleeding in the adolescent is the immature hypothalamic-pituitary-ovarian axis, which causes anovulatory bleeding. No corpus luteum is produced with anovulation; therefore, the ovary secretes no progesterone. However, estrogen production continues. The result is continued endometrial proliferation without progesterone-induced desquamation and stabilization. This produces a disorganized sloughing and repair, leading to abnormal bleeding that can lead to anemia.
Coagulopathies. Coagulopathies in adolescents should be suspected if there are bleeding abnormalities with the onset of the menses. Inherited coagulopathies have been shown to be the underlying cause of abnormal uterine bleeding in approximately 18% of Caucasian and 7% African American patients with menorrhagia.30 Hemophilia A and von Willebrand disease are the two most common inherited disorders of bleeding. The defect, qualitative or quantitative, involves factor VIII-von Willebrand complex. Von Willebrand factor facilitates the adhesion of platelets to subendothelial collagen that prevent bleeding diathesis. Hemophilia A occurs with the deficiency in the amount or activity of factor VIII. Thirty percent of patients will have no family history. Hemophilia B is due to factor IX deficiency and diagnosis is made by assay alone.31 Immune thrombocytopenic purpura (ITP) should also be considered. It usually occurs after a viral illness in children and is characterized by immune mediated platelet destruction. This leads to bleeding abnormalities when the rate of destruction exceeds bone marrow production.32 It is a diagnosis of exclusion and other causes of low platelets have to be investigated.
Pregnancy. All adolescents with abnormal bleeding need to be evaluated to exclude pregnancy. Pregnancy is a common cause of abnormal vaginal bleeding in the sexually active adolescent. It is important to note that adolescents are not forthcoming with this information and care must be taken to make sure there is a level of comfort, privacy, and communication established. Approximately, one third of normal intrauterine pregnancies are associated with bleeding during the first trimester. Abnormal pregnancies such as threatened abortions can be associated with heavy vaginal bleeding. Ectopic pregnancies, which account for 20 out of every 1000 pregnancies, are commonly related with vaginal bleeding and must be excluded in every adolescent.33
Inflammatory Conditions. Sexually transmitted infections are common among adolescents due to inadequate understanding of prevention and lack of proper and timely treatment. Gonorrhea, chlamydia, bacterial vaginosis, and trichomoniasis are common infections that can lead to fulminant cervicitis and vaginitis.
Polycystic Ovarian Syndrome. Another common cause of anovulation is polycystic ovarian syndrome (PCOS), which is a primary ovarian failure. Generally these patients present with some signs of hyperandrogenism (e.g., hirsutism, acne, obesity) Some patients present with follicular cysts on the ovaries, but this is not pathognomic for PCOS; other causes of anovulation may present with cysts on the ovaries. The other clinical feature that may be present includes acanthosis nigricans as an indication of metabolic derangements.34,35 PCOS is associated with unopposed estrogen stimulation, elevated androgen levels, and insulin resistance, and is a common cause of anovulation.
Special Circumstances. Special circumstances must be considered with adolescents who present with abnormal bleeding. Many of the items that are found in the differential diagnosis will have signs and symptoms that are specific to that disease process. Since the spectrum of illness is so broad, narrowing to things that are specific to adolescents and the current presentation will help make the process easier. Many of the items listed in Table 2 may present to the primary doctor and come to the emergency department with the underlying diagnosis in hand. Anovulation in the adolescent can be caused by stress, both emotional and physical, endocrinopathies such as hypothyroidism and diabetes, and primary ovarian failure as with PCOS.24,33,36-38
Diagnosis and Treatment
As important as it is to have a complete and logical differential diagnosis, it is also important to have a synced algorithm for diagnosis and treatment of abnormal bleeding. Table 3 depicts the steps for diagnosis, along with Figure 1 and Figure 2 for evaluation and management.
Table 3. Evaluation |
The evaluation should always begin with a detailed history and physical examination. A general history to include any chronic illnesses and a thorough review of systems to suggest any underlying causes will prevent unnecessary diagnostic testing. There should be a detailed menstrual history that includes menarche as well as last menstrual period, frequency of menses, and descriptions of the "normal" menses for the patient. A sexual history is a must, as well, if possible to obtain the history with and without the parent as the situation allows. A review of confidentiality with the patient is usually a good place to start retrieving this information. Details of the sexual history including any history of sexually transmitted infections, abortions, and the type of sexual activity (i.e., rough sex, penile-vaginal intercourse vs. penile-anal intercourse) A good family history of bleeding disorders, menstrual history (i.e., if anyone had a hysterectomy for bleeding), and other systemic illnesses should be taken.21
The physical examination must include a complete set of vital signs. Orthostatics may be helpful to assess the volume status of the patient. The physical examination can focus the evaluation by pointing to any signs of chronic illness or other underlying condition which is causing the abnormal uterine bleeding. An external genital examination must be performed to evaluate for traumas as mentioned above on all patients. An internal examination should be performed if your history (i.e., admits to sexual activity) and physical examination (i.e., hymen is no longer intact) suggests there is a sexually active female or if there is dysmenorrhea.2,3,21
A thorough skin examination should search for for petechiae, bruising, discoid rashes, and acanthosis nigricans as in PCOS. The history and physical will guide your work up. However, each patient that presents must have at a minimum a CBC, PT, PTT, and pregnancy test. These will also guide what further work up needs to be done. Abdominal and pelvic ultrasounds are only helpful if pursuing the work up of pregnancy and its complications or a mass (i.e., ectopic pregnancy, ovarian mass).2,3,15,21
Special Considerations. Many of the underlying causes will be noted by history and physical examination with minimal work up needed. Endocrine disorders should be suspected in patients with obesity, signs of androgen excess (hirsuitism, acne), thyroid enlargement, galactorrhea (suggests hyperprolactinemia), visual field defects (suggest intracranial, pituitary lesion), ecchymosis or purpura (signs of a bleeding disorder) or signs of anemia or chronic blood loss. A lot of the endocrine disorders listed, if suspected, should have an endocrinologist involved for a comprehensive diagnostic evaluation. If the patient is stable and presents with abnormal uterine bleeding, many of the tests needed to make a definitive diagnosis may not be necessary in the ED and an appropriate referral for a more extensive evaluation may be necessary.
Abuse/Accidents/Foreign Objects. Once sexual abuse is suspected, treatment should be directed toward the injury and protecting the child. The child should be evaluated as per the abuse guidelines for the facility. Reporting abuse is mandatory and should be promptly initiated. Depending on the degree of injury, age of the child and evaluation needed, referral to a child abuse team may be indicated. Also surgical intervention by a pediatric gynecologist or a general gynecologist may be warranted depending on the degree of trauma caused by the abuse. Consult the specific hospital protocol at the facility for guidance with child abuse investigation.
Some accidents, such as minor straddle injuries, are relieved with cold compresses. Care must be taken not to have an ice pack placed directly on the affected tissue in order to prevent thermal injury. If clitoral lacerations are present, but hemostatic, allow them to heal by secondary intention. The clitoris is a highly innervated organ and sutures may cause strictures leading to chronic pain and/or discomfort. Give a periwash bottle and instruction to maintain proper hygiene.
Foreign objects can typically be identified with a basic gynecologic exam. Positioning for a gynecologic exam may vary depending on the comfort level and cooperation of the patient. The dorsal lithotomy position with legs in stirrups is the most common. Other positions include a knee–chest positioning and a "frog-leg" positioning. The prior positions are best used in the young adolescent. If the adolescent is not sexually active and hymen is not intact a light as from an otoscope may be used to perform the exam. A speculum is not always needed, nor appropriate. Internal examination should be completed using index finger. If the removal is unable to be completed in the ED or there are concerns regarding retention of the foreign body, surgical consultation may be needed. Treatment includes the removal of the object and genital hygiene education.
Hypothalamic-Pituitary-Ovarian Dysfunction. Though there are irregularities in the female menstruation cycle in adolescents, intervention is not always needed unless there is underlying anemia. The hypothalamic-pituitary ovarian axis will mature in most adolescents within one to two years. However, in the face of anemia medical management is the gold standard because the underlying problem is hormonal, not structural in adolescents.
For mild anemia, hemoglobin >11 g/dL, a course of NSAIDs may be used to reduce menstrual flow by 20% to 50%. NSAIDs work by blocking prostaglandin formation. Common regimens include, ibuprofen 400 mg three times per day and naproxen sodium 275 mg every 6 hours.16,39-42 Duration of use varies from the first few days of menses to the entire 4-7 days of menses.31,39 The greatest benefit with NSAID therapy is seen with ovulatory bleeding. Concurrent iron replacement is needed until the anemia is corrected.
Acute uterine bleeding with moderate to severe anemia, can be medically managed with conjugated equine estrogen therapy, which facilitates rapid growth of the endometrium. Therapy may be administered by intravenous or oral routes. Intravenous therapy can be administered at 25 mg every 4 hours for 24 hours. Oral therapy is 10-20 mg per day in four divided doses (2.5–5 mg every 6 hours for 24 hours). Both therapies work well. However, intravenous estrogen therapy does not produce the gastrointestinal upset seen in oral therapy and is therefore better tolerated. After 24 hours, start oral contraception 35 micrograms monophasic formulation one tablet by mouth twice daily for one week then allow a withdrawal bleed.11,23,37 The patient should be maintained on combined oral contraception or have induced withdrawal bleeds with progesterone every one to three months. Progesterone therapy allows an organized desquamation of the endometrium and promotes an increased ratio of the PGF2α/PGE.31,43 Over the course of one to three months the anemia is corrected because the progesterone stops excessive proliferation of the endometrium and the prostaglandins cause organized vasoconstriction. In short, there is less surface area to desquaminate and the constriction tamponades the amount and length of bleeding.
Chronic dysfunctional uterine bleeding with moderate anemia can be managed with daily oral contraception use. However, hormonal replacements may delay the maturation of the hypothalamic-pituitary axis in the adolescent. If all above fail, a dilation and curettage may be needed and a gynecologist should be consulted.
Although combined oral contraception is a good option to control abnormal bleeding, be aware that there are risks and patient comorbities that may outweigh the benefit of combined contraception. Adolescents with severe migraines with aura should not take combined contraception because it caused a four-fold increased risk for cerebral vascular accidents. Adolescents with known hypercoagulable states, such as factor V Leiden mutation and systemic lupus erythematosus have higher risk of deep venous thrombosis.44,45 Other hypercoagulable conditions with relative contraindications for the use of combined oral contraception are dyslipidemia and being less than two weeks' postpartum.32,46
Coagulopathies. If a coagulopathy is suspected, screening laboratory studies should be ordered. Coagulopathies are distinguished from hormonal derangements by the time of onset, severity, and other affected organs. For example, a patient with von Willebrand disease might have a history of severe epitaxis and easy bruising presenting with heavy vaginal bleeding with onset of first menses. Von Willebrand disease is clinically recognized by a prolonged bleeding time with normal platelet count. Clinical features of hemophilia A include normal bleeding time and platelet counts with prolonged partial thromboplastin time (PTT) and normal prothrombin time (PT). Diagnosis is by Factor VIII assays only. Hemophilia B is characterized by a prolonged PTT and normal PT and bleeding time.38 Evaluation for ITP would show a normal PT, PTT, and red blood cell count with elevated bleeding time and decreased platelet count (less than 100,000/uL).46 Blood dyscrasias should not be excluded even if the initial workup is negative, especially if this workup is begun while the patient is actively bleeding.25
Pregnancy. Pregnancy is the most common cause of abnormal bleeding and should always be excluded by a urine pregnancy test. Failure to identify risk factors is cited as a common and significant reason for misdiagnosis of ectopic pregnancy. A proper history and physical examination remain the foundation for initiating an appropriate workup that will result in the accurate and timely diagnosis of an ectopic pregnancy. Identification of risk factors can raise the index of suspicion and lend significance to otherwise minor physical findings. For example, subtle changes in vital signs, such as mild tachycardia or lower than usual blood pressure, should prompt further investigation. Scoring systems have been proposed to facilitate earlier diagnosis of ectopic pregnancy by indicating the level of risk as a function of weighted risk factors.
After a careful history and physical examination, ancillary studies may include a urine pregnancy test and determination of the serum progesterone level and serum quantitative β-hCG levels. The standard urine pregnancy test is 99% sensitive and 99% specific for pregnancy. If positive and there is an unsure last menstrual cycle a quantitative human chorionic gonadotropin assay should be ordered. An intrauterine pregnancy can be identified by ultrasound with quantitative hcg of 1,500 to 2,000 mIU/mL. An ultrasound is needed to rule in an intrauterine pregnancy. If one is not identified and the Qhcg values are 1,500 to 2,000 mIU/mL, an ectopic pregnancy should be assumed. At this point, consultation with gynecology should take place.11,36 Although used as the initial step in some settings, the urine pregnancy test is a qualitative rather than quantitative measure that identifies the presence of hCG in concentrations as low as 25 mIU per mL. Historically, serum progesterone levels were obtained concurrently with β-hCG levels. Some clinicians continue to find progesterone determinations useful. The rationale is that viable intrauterine pregnancies were associated with serum progesterone levels of 11 ng per mL (35 nmol/L) or greater in one study, and levels of 25 ng per mL (80 nmol/L) or greater in another study. Corresponding sensitivities were 91% at 11 ng per mL47 and 97.5% at 25 ng per mL. Ultrasonography is routinely utilized in these situations. The discriminatory zone is the range of serum β-hCG concentrations above which a gestational sac can be visualized consistently. Abdominal ultrasonography should consistently detect the gestational sac when the β-hCG level is greater than 6,500 mIU per mL (6,500 IU per L). Absence of an intrauterine gestational sac on abdominal ultrasound in conjunction with a b-hCG level of greater than 6,500 mIU per mL suggests the presence of an ectopic pregnancy. Compared with abdominal ultrasonography, transvaginal ultrasonography diagnoses intrauterine pregnancies an average of one week earlier because it is more sensitive and has a lower discriminatory zone (i.e., a β-hCG level between 1,000 and 1,500 mIU per mL [1,000 and 1,500 IU per L]). An ectopic pregnancy can be suspected if the transvaginal ultrasound examination does not detect an intrauterine gestational sac when the β-hCG level is higher than 1,500 mIU per mL.
Inflammatory Conditions. Untreated sexually transmitted infections causing cervicitis and vaginitis should be identified and treated with the appropriate antibiotic. During the examination of a sexually active adolescent, a screening test that utilizes DNA PCR and wet prep should be taken. The DNA probe will identify gonorrhea and chlamydia. However, the results are not immediate. Therefore, if there is a high level of suspicion for pelvic inflammatory disease, ceftriaxone 250 mg intramuscular and doxycycline 100 mg twice-daily oral dose for seven days should be given with or without metronidazole.48 If results are known and gonorrhea is detected by the genprobe but not chlamydia, the patient should still be treated for chlamydia because there is a high incidence of false negative results. The wet prep will identify trichomoniasis, bacterial vaginitis, and candidal infections. Trichomonaisis should be treated with 2 gm of metronidazole by mouth (times one). Bacterial vaginitis should be treated with metronidazole 500 mg bid for seven days. Alternative regimes, including the antibiotic therapy for pregnancy, can be found in the 2006 Centers for Disease Control Guidelines for the Treatment of Sexually Transmitted Infections.48
Prognosis
The patient generally does well and can self regulate after a period of time. Upon discharge from the emergency room, the patient should see her primary physician in one or two days. The patient and parent may need a lot of reassurance upon discharge. Patients with underlying conditions may continue to have issues as their disease process progresses.49,50
Conclusion
Abnormal bleeding creates great apprehension when it affects adolescents. The premises are the same for adults and adolescents: A good history and physical exam. A synced differential diagnosis and treatment algorithm is key for management of these adolescent patients. Special considerations such as abuse are always important but should not overshadow other possibilities. Menses is the last stage of an organized chaos — puberty.
If no morbidities exist, the best form of therapy is patience. If there are bleeding abnormalities due to an organic cause, then treatment of that underlying disease process is first in order. If the hypothalamic-pituitary-ovarian axis immaturity is the cause for concern, then the gold standard is medical management if there is concern about progression of the dysfunctional bleeding.
References
1. Houston AM, Abraham A, Huang Z, et al. Knowledge, attitudes, and consequences of menstrual health in urban adolescent females. J Pediatr Adolesc Gynecol 2006;19:271-275.
2. Strickland JL, Wall JW. Abnormal uterine bleeding in adolescents. Obstet Gynecol Clin N Am 2003;30:321-335.
3. Matystina LA, Zoloto EV, Sinenko LV, et al. Dysfunctional uterine bleeding in adolescents: Concepts of pathophysiology and management. Prim Care Clin Office Pract 2006;33:503-515.
4. Minjarez DA, Bradshaw KD. Abnormal uterine bleeding in adolescents. Obstet Gynecol Clin N Am 2002;27:63-78.
5. Mitan LA, Slap GB. Dysfunctional uterine bleeding. In: Neinstein LS, Ed. Adolescent Health Care – A Practical Guide. 4th ed. Philadelphia: Lippincott Williams and Wilkins;2002:966-972.
6. LeMarchand-Beraud T, Zufferey MM, Reymond M, et al. Maturation of the hypothalamo-pituitary-ovarian axis in adolescent girls. J Clin Endo Metab 1982;54(2):241-246.
7. Greenfield TP, Blythe MJ. Menstrual disorders in adolescents. In: Greydanus DE, Patel Dr, Pratt HD, Eds. Essential Adolescent Medicine. New York: McGraw-Hill Medical Publishers; 2006:591-612.
8. Cotran RS, KumarV, Collins T, et al. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia: W.B. Saunders Co.;1999:638-640.
9. Shwayder JM. Contemporary management of abnormal uterine bleeding. Pathophysiology of abnormal uterine bleeding. Obstet Gynecol Clin North Am 2000;27:219-234.
10. Sanfilippo JS, Hertweck SP. Physiology of menstruation and menstrual disorders. In: Friedman SB, Fisher MM, Schonberg SK, et al Eds. Comprehensive Adolescent Health Care. 2nd ed. St. Louis, MO.: Mosby; 1998:990-1017.
11. Chabbert-Buffet N, Djakoure C, Maitre SC, et al. Regulation of the human menstrual cycle. Front Neuroendocrinol 1998;19:151.
12. Chumlea WC, Schuber CM, Roche AF, et al. Age at menarche and racial comparisons in US girls. Pediatrics 2003;111:110.
13. Collett TF. Irregular uterine bleeding in adolescents. J Pediatr Health Care 2002;16:313, 321-322.
14. Livingstone M, Fraser JS. Mechanism of abnormal uterine bleeding. Hum Reprod Update 2002;8: 60-67.
15. Lavin C. Dysfunctional uterine bleeding in adolescents. Curr Opin Pediatr 1996;36:156-159.
16. Speroff L, Glass RH, Kase NG, eds. Dysfunctional uterine bleeding. In: Clinical Gynecologic Endocrinology and Infertility. 5th ed. Baltimore: Williams and Wilkins; 1994:575-593.
17. Fraser, IS, Hickey M, Song JY. A comparison of mechanisms underlying disturbances of bleeding caused by spontaneous dysfunctional uterine bleeding or hormonal contraception. Hum Repod 1996;11:165-178.
18. Deligeoroglou EK. Dysfunctional uterine bleeding. Annals of the New York Academy of Sciences 1997;816(1):158-164.
19. Slap GB. Menstrual disorders in adolescence. Best Pract Res Clin Obstet Gynaecol 2003;17(1):75-92.
20. Templeman C, Paige Herweck PS, Muram D, et al. Vaginal bleeding in childhood and menstrual disorders in adolescence. In: Sanfilippo S, Muram D, Lee, PA, et al., Eds. Pediatric and Adolescent Gynecology. Philadelphia: WB Saunders Co; 2001: 34-40
21. Rimsza ME. Dysfunctional uterine bleeding. Peds Rev 2002;23:
227-233.
22. Iglesia EA, Coupey SM. Menstrual cycle abnormalities: Diagnosis and management. Adolescent Medicine: State of the Art Reviews 1999;10:255-274
23. Smith SK, Abel, MK, Kelly RW, et al. The synthesis of prosta-glandins from persistent proliferative endometrium. J Clin Endocrinol Metab 1982;55:284-289
24. Brenner PF. Differential diagnosis of abnormal uterine bleeding. Am J Obstet Gynecol 1996;175:766-769.
25. Jayasinghe Y, Moore P, Donath S, et al. Bleeding disorders in teenagers presenting with menorrhagia: Australian and New Zealand. J Obstet Gynaecology 2005;45:439-443.
26. Heppenstall-Heger A, McConnell G, Ticson L, et al. Healing patterns in anogenital injuries: A longitudinal study of injuries associated with sexual abuse, accidental injuries, or genital surgery in the preadolescent child. Pediatrics 2003;112:829-837.
27. Adams JA. Evolution of a classification scale: Medical evaluation of suspected child sexual abuse. Child Maltreatment 2001;6:31-36.
28. Emans SJ. Sexual abuse. In: Emans SJ, Laufer MR, Goldstein DP, Eds. Pediatric and Adolescent Gynecology. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1998:751-794.
29. American College of Obstetrics and Gynecology Practice Bulletin. Clinical management guidelines for obstetricians-gynecologists. Use of botanicals for management of menopausal symptoms. Obstet Gynecol 2001;97:630-636.
30. Dilley A, Drews C, Millins C, et al. Von Willebrand disease to the inherited bleeding disorders in women with diagnosed menorrhagia. Obstet Gyn 2001;97:630-636.
31. Kilbourn L, Richards S. Abnormal uterine bleeding: Diagnostic considerations, management options. Postgrad Med 2001;109:1.
32. Petri M, Robinson C. Oral contraceptives and systemic lupus erythematosus. Arthritis Rheum 1997;40:797-803.
33. Chow WH, Daling JR, Cates W Jr, et al. Epidemiology of ectopic pregnancy. Epidemiol Rev 1987;9:70-94.
34. Barbieri RL, Gargiulo AR. Metformin for the treatment of the polycystic ovary syndrome. Minerva Ginecol 2004;56:63-79.
35. Stadtmauer LA, Wong BC, Oehninger S. Should patients with polycystic ovary syndrome be treated with metformin: Benefits of insulin sensitizing drugs in polycystic ovary syndrome-beyond ovulation induction. Human Reprod 2002;17:3016-3025.
36. Kilbourn CL, Richards, CS. Abnormal uterine bleeding. Postgrad Med 2001;109:137-150.
37. Petrozza J, Poley, K. Dysfunctional uterine bleeding. In: Curtis MG, Hopkins MP, Eds. Glass's Office Gynecology. 5th ed. Baltimore: Williams and Wilkins; 1999;241-264.
38. Kadar N, Caldwell BV, Romero R. A method of screening for ectopic pregnancy and its indications. Obstet Gynecol 1981;58:162-166.
39. Davis A, Godwin A, Lippman J, et al. Triphasic norgestimate-ethinyl estradiol for treating dysfunctional uterine bleeding. Obstet Gynecol 2000;96:913-920.
40. Rosenfeld JA.Treatment of menorrhagia due to dysfunctional uterine bleeding. Am Fam Physician 1996;53(1):165-172
41. Demir SC, Kadayyfcy TO, Vardar MA, et al. Dysfunctional uterine bleeding and other menstrual problems of secondary school students in Adana, Turkey. J Pediatr Adolesc Gynecol 2000;13:171-175.
42. Chen BH, Giudice LC. Dysfunctional uterine bleeding. West J Med 1998;169:280-284.
43. Emans SJ. Delayed puberty and menstrual abnormalities. In: Emans SJ, Laufer MR, Goldstein DP, Eds. Pediatric and Adolescent Gynecology. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1998:163-262.
44. Stenchever MA, Droegemueller W, Hervst AL, et al. Comprehensive Gynecology. 4th ed. Philadelphia: Mosby; 2001:1083, 1087, 1100.
45. Smith SK, Abel MH, Kelly RW, et al. The synthesis of prostaglandins from persistent proliferative endometrium. J Clin Endocrinol Metab 1982;55:284.
46. Price DT, Ridker PM. Factor V Leiden mutation and the risks for thromboembolic disease: A clinical perspective. Ann Intern Med 1997;127:895-903.
47. Rosenfield RL. Hyperandrogenism in prepubertal girls. Pediatr Clin North Am 1990;37:1333-1358.
48. Centers for Disease Control and Prevention. CDC Guidelines for the Treatement of Sexually Transmitted Infections, 2006.
49. Southam AL, Richart RM. The prognosis for adolescent girls with menstrual abnormalities. Am J Obstet Gynecol 1966;94:637-645.
50. Elford KJ, Spence JE. The forgotten female: Pediatric and adolescent gynecological concerns and their reproductive consequences. J Pediatr Adolesc Gynecol 2002;15:65-77.
It is very common for adolescent females to present with menstrual irregularities and differentiating normal variations from life-threatening problems is critical to the emergency department physician.Subscribe Now for Access
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