INTRODUCTION — Uterine adenomyosis is a disorder in which endometrial glands and stroma are present within the myometrium (uterine musculature), resulting in hypertrophy of the surrounding myometrium. Patients with symptomatic adenomyosis present with uterine enlargement, abnormal uterine bleeding, and painful menses. Consideration of adenomyosis is part of the evaluation of these symptoms.
The diagnosis and management of uterine adenomyosis will be reviewed here. Other topics related to uterine pathology and abnormal uterine bleeding are presented separately. (See "Abnormal uterine bleeding in nonpregnant reproductive-age patients: Terminology, evaluation, and approach to diagnosis" and "Abnormal uterine bleeding in nonpregnant reproductive-age patients: Management" and "Uterine fibroids (leiomyomas): Epidemiology, clinical features, diagnosis, and natural history".)
HISTOPATHOLOGY — There are two forms of adenomyosis: diffuse and focal.
●Diffuse adenomyosis – On gross inspection, the uterus with diffuse adenomyosis is uniformly enlarged and boggy, in contrast to the irregular and firm appearance of the fibroid uterus, although the two conditions (fibroids and adenomyosis) can occur concurrently. The average uterine weight is usually between 80 and 200 grams, unless coexisting leiomyomas are present. Upon sectioning the uterus, the myometrial wall appears thickened and often contains small hemorrhagic or chocolate-colored areas representing islands of endometrial bleeding.
●Focal adenomyosis (also called adenomyoma) – On gross inspection, focal adenomyosis can resemble a fibroid but without the pseudocapsule that allows for easy enucleation of leiomyomas at surgery.
The term "cystic" is used to describe either diffuse adenomyosis or adenomyomas for which cysts ≥1 cm in diameter are seen on imaging studies. The entity "juvenile cystic adenomyoma" has been used to describe a syndrome in which females 30 years or younger with severe dysmenorrhea have myometrial cysts ≥1 cm [1]. However, cystic adenomyosis has been reported in females of a variety of reproductive ages [2].
The pathognomonic feature of adenomyosis is the presence of endometrial tissue within the myometrium at a distance of at least one low-power field (some authorities insist on two low-power fields) from the endomyometrial junction. The distance requirement is to preclude mistaking the normal endometrium between muscle fibers at the mucosa for adenomyosis when the specimen is transected for slide preparation. A prior history of endometrial ablation could confound the diagnosis of adenomyosis as the procedure distorts or destroys the endometrial/myometrial junction.
The ectopic endometrium usually has an immature proliferative pattern.
PATHOGENESIS — The pathogenesis of adenomyosis is not known. The two major theories are that it either develops from endomyometrial invagination of the endometrium or de novo from müllerian rests [3]. A mouse model of adenomyosis and molecular studies support the invagination hypothesis, facilitated by weakness of degenerating uterine smooth muscle tissue [4,5]. However, a metaplastic process appears to be more likely given a report of adenomyosis in a woman with Rokitansky-Kuster-Hauser syndrome who lacked eutopic endometrium [6]. There is also increasing molecular evidence that the adenomyotic glands differ in expression of key molecules from eutopic endometrial glands [7-11].
There is also evidence that the junctional zone of the myometrium may play a key role in this disease [12]. The junctional zone is a region appearing as a dark band on T2-weighted magnetic resonance imaging that separates the subendometrial myometrium from the outer myometrium but cannot be identified histologically. Studies show this region has ultrastructural changes and differential growth factor expression that may influence physiology [13-15].
Estrogen and progesterone appear to play a role in adenomyosis pathophysiology as they do in other gynecologic disorders. This is primarily inferred from the response of symptoms to steroidal treatments. There are studies that suggest that estrogen is produced in adenomyotic tissue and in vitro studies that suggest that aromatase in the endometrium of patients with adenomyosis is normalized by gonadotropin-releasing hormone agonist and danazol treatment, but not studies of direct action on adenomyotic implants [16,17]. A murine model of adenomyosis suggests that early exposure to estrogen (in this experiment, tamoxifen) led to an increased risk of adenomyosis and abnormal myometrium, which also supports the invagination hypothesis [18].
Other animal models suggest that pituitary protein hormones, including prolactin, follicle-stimulating hormone, and oxytocin, which have direct uterine effects, may also have roles in the pathogenesis of this disorder [4,19-24]. Both direct exposure of the uterus to prolactin and hyperprolactinemia secondary to selective serotonin reuptake inhibitor use appear capable of inducing uterine adenomyosis [25]. This hypothesis is strengthened by research showing both depression and antidepressant use are increased in patients with adenomyosis and there is some treatment response to dopamine agonists [26,27]. However, this association could be a result of chronic pain as well.
There is some evidence that adenomyosis and leiomyomas share elements of pathogenesis such as growth factor dysregulation and abnormalities of angiogenesis [10,28-32]. In model systems, the efficacy of some conventional and investigational therapies may be mediated through these systems [17,33].
Although adenomyosis and endometriosis both represent disorders of ectopic endometrium and can be a cause of pelvic pain, the two diseases are not thought to be otherwise related. (See "Endometriosis: Pathogenesis, epidemiology, and clinical impact".)
EPIDEMIOLOGY AND RISK FACTORS — The natural history, prevalence, and risk factors of adenomyosis are uncertain because the definitive diagnosis can only be made on pathology evaluation, typically following hysterectomy, although a clinical diagnosis can be made with imaging studies. Thus, much that we know about the epidemiology of adenomyosis may, in fact, be the epidemiology of hysterectomy.
It is generally estimated that adenomyosis is present in 20 to 35 percent of females [34,35]. Higher rates have been reported; the incidence was approximately 65 percent in one study in which meticulous histopathologic analysis of multiple myometrial sections was performed [36]. Since the total number of cases is unknown, there is no reliable estimate of the proportion of patients who develop symptoms or undergo hysterectomy.
In terms of age of onset and progression of disease, adenomyosis has been found in adolescents in studies that use pelvic imaging rather than hysterectomy for diagnosis [37,38]. Most patients undergoing hysterectomy for adenomyosis are in their later reproductive years.
Adenomyosis appears to be more common in parous than nulliparous patients [36,39,40]. However, a greater number of pregnancies are not associated with a higher risk of the disease [41]. The relationship between parity and adenomyosis may be biased since the diagnosis is typically made only at hysterectomy. Interestingly, the situation is just the opposite in patients with leiomyomas, in whom parity is associated with a decreased risk of disease.
Adenomyosis often coexists with other uterine diseases, primarily uterine leiomyomas and endometriosis, and this makes it difficult to determine whether adenomyosis has unique risk factors or even how it behaves as a disease. As an example, persistence of pelvic pain following optimal endometriosis surgical therapy may be confounded by the presence of adenomyosis [37,42].
On the other hand, one study argued that adenomyosis was a normal variant and not a true disease because the presenting symptoms for hysterectomy were similar with and without the finding of adenomyosis [39]. However, at the time of recruitment, all patients were at least 42 years old, and as they were followed for 10 years, the cohort represented only perimenopausal patients.
Other studies suggest, however, that patients with adenomyosis do differ from patients with other disease processes. A longitudinal study recruiting females starting at age 22 found that, compared with patients with endometriosis, patients with adenomyosis had increased parity, early menarche, and shorter menstrual cycles [40]. One-half of the patients in both groups had concomitant leiomyomas [40].
A case-control study compared patients undergoing hysterectomy in whom leiomyomas were found on pathologic examination and matched them to patients in whom only adenomyosis was found [26]. In this study, patients with adenomyosis were significantly younger and were more likely to have dysmenorrhea, pelvic pain, depression, and a history of prior uterine surgery [26]. In a multivariate analysis confined to patients with uteri weighing more than 150 grams, patients with adenomyosis were more likely to have depression and endometriosis compared with patients with only fibroids [26].
Several additional studies have reported that prior uterine surgery may be a risk factor for adenomyosis [26,43].
A large population-based study reported that adenomyosis is associated with an increased risk of both endometrial and thyroid cancers, with hazard ratios of 2.19 (95% CI 1.51-3.16) and 1.70 (95% CI 1.29-2.24), respectively [44]. Confirmation of this finding in other populations after adjustment for clinical risk factors would likely impact screening for these diseases.
CLINICAL PRESENTATION — Heavy menstrual bleeding and dysmenorrhea are the typical symptoms of adenomyosis, occurring in approximately 60 and 25 percent of patients, respectively [36]. Chronic pelvic pain may also occur.
Heavy menstrual bleeding is possibly related to the increased endometrial surface of the enlarged uterus, while pain may be due to bleeding and swelling of endometrial islands confined by myometrium. There is also evidence that menstrual blood loss is correlated with the overexpression of inflammatory mediators in adenomyotic tissue samples [45]. Approximately one-third of patients are asymptomatic.
Symptoms are typically reported to develop between the ages of 40 and 50 years; however, this may reflect the fact that most adenomyosis has historically been diagnosed at hysterectomy, and younger patients are less likely to undergo definitive reproductive surgery. Reports using magnetic resonance imaging (MRI) criteria for diagnosis suggest that the disease may cause dysmenorrhea and chronic pelvic pain in more adolescents and younger reproductive-age patients than previously appreciated [37,42]. In contrast with endometriosis, dyspareunia is not a typical symptom.
One epidemiologic study noted an increased risk of preterm birth in patients with adenomyosis, which was diagnosed by either ultrasound or MRI [46]. This association may have been related to confounders or misdiagnosis of the disease; confirmation is required.
It is controversial whether adenomyosis is linked to infertility. There are many confounding issues including the fact that hysterectomy is required for definitive diagnosis, endometriosis commonly coexists, and most evidence comes from small case series [47,48]. However, in a study of baboons, lifelong infertility was strongly associated (20-fold increased odds) with histologic adenomyosis even when concomitant endometriosis was excluded [49]. A meta-analysis of studies examining adenomyosis in patients undergoing in vitro fertilization suggests adenomyosis-impaired fertility and that use of pretreatment gonadotropin-releasing hormone agonist may be beneficial [50]. Finally, adenomyosis may also be associated with increased pregnancy complications, including miscarriage and preterm birth [51,52].
Most patients with this disorder have another pathologic process in the uterus that often obscures the diagnosis of adenomyosis and makes the delineation of a symptom profile for "pure" adenomyosis difficult. In one review, as an example, leiomyomas, endometriosis, and endometrial polyps were also present in 50, 11, and 7 percent, respectively, of patients with adenomyosis [36]. In another study, adenomyosis was suspected on MRI in up to 90 percent of patients with endometriosis [53].
EVALUATION — Patients with suspected adenomyosis are evaluated with history, pelvic examination, and imaging. Laboratory testing may be performed to evaluate for anemia.
History — A medical history is taken, including the obstetric and gynecologic history and the relevant medical history. Other conditions or medications that may cause heavy menstrual bleeding or pelvic pain should be included.
Pelvic examination — The bimanual pelvic examination in patients with adenomyosis typically shows a uterus that is mobile, diffusely enlarged (often referred to as "globular" enlargement), and soft (often referred to as "boggy").
The uterus only rarely exceeds the size of a pregnant uterus at 12 weeks of gestation [54]. However, some patients have a normal sized uterus, and others develop masses (termed adenomyomas), which clinically resemble leiomyomas. The uterus may be tender.
Adenomyosis does not result in a fixed uterus, but this may occur with endometriosis, which also often co-occurs with adenomyosis.
Laboratory tests — There are no laboratory tests to diagnose adenomyosis. A urine or serum human chorionic gonadotropin should be measured to exclude pregnancy in reproductive-age patients with uterine enlargement, abnormal uterine bleeding, or pelvic pain. A hemoglobin/hematocrit may be ordered if the patient has heavy menstrual bleeding and anemia is suspected.
If pelvic pain is present, tests to exclude infection may be sent, if appropriate.
Imaging — Transvaginal ultrasound (TVUS) is the first-line imaging choice for evaluation of an enlarged uterus, pelvic pain, and/or abnormal bleeding (image 1). The images should be reviewed by a radiologist or gynecologist experienced in evaluating adenomyosis.
Magnetic resonance imaging (MRI) is reserved for those cases in which it is important to distinguish diffuse and focal adenomyosis from leiomyomas and those cases when an accurate diagnosis is important to determine management (image 2) [55]. If the patient is planning conservative surgery for adenomyosis or fibroids, an MRI is often performed to assist in surgical planning. In a meta-analysis including over 3300 patients with adenomyosis confirmed on hysterectomy specimen, the sensitivity and specificity of MRI for diagnosing adenomyosis were 71 and 91 percent, as compared with 81 and 87 percent for TVUS [56].
Signs of adenomyosis on both imaging modalities include asymmetric thickening of the myometrium (with the posterior myometrial typically thicker), myometrial cysts (image 3), linear striations radiating out from the endometrium, loss of a clear endomyometrial border, and increased myometrial heterogeneity [57]. With MRI, some quantitation of the thickening of the junctional zone is possible, with >12 mm generally considered diagnostic of the disease and <8 mm excluding adenomyosis [57], although the upper cutoff has been questioned [58].
There is no standard for determining when a diagnostic threshold is met for an image-based diagnosis of adenomyosis. There has been some discussion that thickening of the junctional zone (termed "junctional zone hyperplasia") or endometrial-subendometrial myometrium unit disruption (which includes disruption as well as thickening of the junctional zone) may be either distinct clinical entities or early manifestations of adenomyosis [59,60]. However, studies on the natural history of adenomyosis are lacking. This thickening of the junctional zone can be confused with thickened endometrium in some imaging reports. Thus, clinically, the diagnosis of adenomyosis should be considered when scant tissue is obtained following an endometrial biopsy of thickened endometrium.
The only study on use of computed tomography for diagnosis of adenomyosis showed poor diagnostic accuracy [61].
In patients undergoing treatment with tamoxifen, a pattern consistent with adenomyosis may be seen [62]. Because these cases are mostly of postmenopausal patients, it appears likely a consequence of the agonistic effects of tamoxifen; pathologic examination has not been reported with these cases. (See "Abnormal uterine bleeding and uterine pathology in patients on tamoxifen therapy", section on 'Pelvic ultrasound and endometrial sampling'.)
Other tests — Endometrial biopsy is not informative in the diagnosis of adenomyosis since it is a myometrial disease. However, it is often required in patients under evaluation for adenomyosis since they have abnormal uterine bleeding and endometrial hyperplasia or carcinoma must be excluded (table 1).
Needle biopsy of the myometrium is not a common practice and is reserved for clinical situations in which a malignancy needs to be excluded. Sensitivity of needle biopsy depends upon several factors, including the extent of disease, number of biopsy specimens obtained, sampling site, needle gauge, and operator experience [54].
DIAGNOSIS — Uterine adenomyosis is a histologic diagnosis made based on pathology evaluation of the uterus after hysterectomy.
The preoperative diagnosis is suggested by characteristic clinical manifestations (ie, heavy menstrual bleeding and dysmenorrhea with a uniformly enlarged uterus), and a clinical diagnosis can be made with transvaginal ultrasound or magnetic resonance imaging findings.
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of adenomyosis includes other conditions associated with abnormal uterine bleeding (AUB (table 2 and table 3)) or dysmenorrhea (table 4). Negative pregnancy testing excludes conditions associated with bleeding during pregnancy. (See "Causes of female genital tract bleeding".)
AUB is caused by many conditions. Patients should be evaluated for uterine cancer, as appropriate. (See "Abnormal uterine bleeding in nonpregnant reproductive-age patients: Terminology, evaluation, and approach to diagnosis" and "Endometrial carcinoma: Clinical features, diagnosis, prognosis, and screening" and "Uterine sarcoma: Classification, epidemiology, clinical manifestations, and diagnosis".)
Uterine leiomyomas may cause heavy menstrual bleeding; these tend to cause noncyclic pelvic pain or pressure but may also be associated with dysmenorrhea. Pelvic imaging can detect leiomyomas, but fibroids may also coexist with adenomyosis, and if a patient has both, it can be difficult to know which is the cause of the symptoms. Also, endometrial polyps cause AUB, but this tends to be intermenstrual bleeding; these may also be visualized on ultrasound. (See "Uterine fibroids (leiomyomas): Epidemiology, clinical features, diagnosis, and natural history" and "Endometrial polyps".)
Patients with endometriosis classically present with dysmenorrhea, dyspareunia, and infertility. Endometriosis usually requires surgery for diagnosis, but some patients develop an ovarian endometrioma with a characteristic appearance on ultrasound. Patients with persistent pain following adequate treatment for endometriosis may have adenomyosis as an underlying diagnosis [42]. (See "Endometriosis: Pathogenesis, epidemiology, and clinical impact".)
Chronic endometritis is a less common cause of AUB and dysmenorrhea and is diagnosed with endometrial biopsy. Patients with pelvic inflammatory disease have acute or subacute pelvic pain; they may present with cervical discharge or fever and typically do not present with AUB. (See "Endometritis unrelated to pregnancy", section on 'Chronic endometritis' and "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)
MANAGEMENT
Hysterectomy — Hysterectomy is the definitive treatment for adenomyosis. Since disease is confined to the uterine corpus, the ovaries may be conserved.
The procedure for hysterectomy is the same as for other benign indications and may be performed via laparotomy, transvaginal, laparoscopy, or robotic surgery. (See "Hysterectomy for benign indications: Selection of surgical route" and "Abdominal hysterectomy" and "Laparoscopic hysterectomy" and "Vaginal hysterectomy".)
Hysterectomy is the only way to remove diffuse adenomyosis. Even in patients with adenomyomas, hysterectomy is generally preferred to removal of the adenomyomas with uterine conservation except where future pregnancy is desired.
In contrast to uterine myomas, which can be readily shelled out from the surrounding myometrium, adenomyomas are not easily excised, and, often, a surgical plane cannot easily be developed and sharp dissection is required. Furthermore, the consistency of the adenomyotic uterus is described as "woody," and suturing is difficult in this environment.
Alternatives
Hormonal medications — For patients who have not completed childbearing, hormonal treatment may be effective for reducing heavy menstrual bleeding and dysmenorrhea, as in endometriosis. (See "Endometriosis: Treatment of pelvic pain".)
In our practice, the preferred treatment is a levonorgestrel (LNG)-releasing intrauterine device (IUD) given its direct action on the uterus, low systemic levels of steroid hormones, and long-acting user-independent administration. The LNG IUD has been shown to improve adenomyosis-associated heavy menstrual bleeding and dysmenorrhea [63-65]. One small study observed a 24 percent reduction in the thickness of the junctional zone (subendometrial myometrium) on magnetic resonance imaging (MRI) as well as a reduction in pain and abnormal bleeding in most patients after six months of use of the LNG IUD [66].
While estrogen-progestin contraceptives are frequently used as primary treatment for dysmenorrhea, there are little data on the efficacy of these contraceptives specifically for adenomyosis. In a small randomized trial, use of both combined oral contraceptives and the LNG IUD was no more effective for reducing pain and bleeding than use of the LNG IUD alone [67].
Other options include oral dienogest (available outside the United States as a single agent), which requires daily administration; depot gonadotropin-releasing hormone (GnRH) analogs; aromatase inhibitors; and the oral GnRH antagonist elagolix, which has been used for treatment of adenomyosis alone and for treatment of uterine fibroids with concomitant adenomyosis [68-73].
When hormonal medications are discontinued, for example when a patient wants to conceive, enlargement of the uterus and recurrence of symptoms are usually documented within six months after discontinuation.
Uterine artery embolization — For patients who have completed childbearing, uterine artery embolization (UAE) may be effective for reducing symptoms related to adenomyosis. UAE is also an option for patients who decline, or have contraindications to, a hysterectomy or have failed hormonal treatment. (See "Uterine fibroids (leiomyomas): Treatment with uterine artery embolization", section on 'Reproductive outcomes'.)
Studies on UAE for adenomyosis show a 25 percent reduction in uterine volume and clinical improvement in heavy menstrual bleeding and overall symptom reduction (image 4) [74-78].
●The largest study followed 264 patients with adenomyosis treated with UAE, of whom 252 completed 12 months of follow-up and 195 completed five years of follow-up; median age at treatment was 38 years (range 28 to 51 years) [79]. Approximately 1.5 percent (4 of 264) had failed embolization, 3.0 percent (7 of 264) had premature ovarian insufficiency diagnosed within three months of the procedure, and there was one periprocedural death due to a pulmonary embolus. From one to five years, an additional 22 percent (57 of 264) of the cohort was lost to follow-up, nine had hysterectomies, and three died of other causes. Among the cohort that completed five years of follow-up, approximately 70 percent of patients had improvement in painful and heavy menses and that improvement was greatest in patients with hypervascular lesions as determined by digital subtraction angiography at the time of treatment [79].
However, some data demonstrate high failure rates, with patients requiring additional intervention for persistent or recurrent symptoms. Pathologic examination of uteri two years after UAE has revealed viable foci of adenomyosis, which may explain these high failure rates [74].
Uterus-sparing resection — Uterus-sparing resection of adenomyosis is an investigational approach that can be considered in patients with extensive adenomyosis who are actively pursuing pregnancy [80]. The disadvantage of this approach is that even when performed by expert surgeons, the rate of uterine rupture in a future pregnancy appears to be 4 percent and has been reported to occur between 12 and 35 weeks of gestation [81]. This rate exceeds the uterine rupture rate after myomectomy or classical cesarean birth (estimated risk of rupture with labor after classical cesarean: 2 percent [82]). Other pregnancy complications, such as abnormal placental attachment, have also been reported. Patients who undergo uterus-sparing resection should be managed during a future pregnancy even more conservatively than patients who have had other transmyometrial surgery and are candidates for prelabor cesarean birth. (See "Cesarean birth: Preoperative planning and patient preparation", section on 'Scheduling' and "Repeat cesarean birth", section on 'Timing'.)
A preoperative MRI is obtained to evaluate the location and extent of the adenomyosis, determine if uterus-sparing surgery is feasible, and help the surgeon plan the procedure. Both laparoscopic and laparotomy techniques have been utilized, often using laparoscopy for focal adenomyosis and an open approach for diffuse adenomyosis [81]. Surgical techniques include wedge resection of the uterine wall, transverse H-incision on the uterine fundus with resection of the adenomyosis, and Osada triple-flap method. Following uterus-sparing surgery, patients who desire pregnancy will often undergo in vitro fertilization to optimize the chance of conception prior to disease recurrence.
In a meta-analysis of 12 studies on outcomes after uterus-sparing surgery for the treatment of adenomyosis, partial and complete excision of adenomyosis were associated with improvement of pain and menorrhagia and reduction in uterine volume [83]. Of the 364 patients who attempted to conceive, 35 percent were successful, and, of those, 18 percent miscarried, 7 percent delivered preterm, and 74 percent had a full-term birth. One uterine rupture occurred (1/126 or 0.8 percent).
After uterine-sparing resection is performed, hormonal agents, such as GnRH agonists and the LNG IUD, are often used to prevent recurrence and control symptoms [84,85].
Other treatments — Other uterine-sparing interventions more commonly used for uterine fibroids show some efficacy for treatment of adenomyosis. Case series of both ultrasound- or MRI-guided focused ultrasound surgery, the latter with the device approved for uterine fibroid treatment, show both symptom improvement and uterine volume reduction with 6 to 12 months of follow-up [86-89].
Reports of laparoscopic radiofrequency ablation of uterine adenomyosis with the same device approved for uterine fibroid treatment and transcervical radiofrequency ablation with a device only available in China suggest some efficacy in terms of short-term symptom improvement and volume reduction [90,91].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Abnormal uterine bleeding".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Uterine adenomyosis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Pathogenesis – Uterine adenomyosis is a disorder in which endometrial glands and stroma are present within the myometrium (uterine musculature). The ectopic endometrial tissue appears to induce hypertrophy and hyperplasia of the surrounding myometrium, which results in a diffusely enlarged uterus (often termed "globular" enlargement) analogous to the concentric enlargement of the pregnant uterus. (See 'Introduction' above and 'Pathogenesis' above.)
●Epidemiology – It is generally estimated that adenomyosis is present in 20 to 35 percent of females, although the prevalence is uncertain since hysterectomy is required to make a definitive diagnosis. (See 'Epidemiology and risk factors' above.)
●Clinical presentation and findings – Heavy menstrual bleeding and dysmenorrhea are the typical symptoms of adenomyosis, occurring in approximately 60 and 25 percent of patients, respectively. Chronic pelvic pain may also occur. The bimanual pelvic examination in patients with adenomyosis typically shows a uterus that is mobile, diffusely enlarged (often referred to as "globular" enlargement), and soft (often referred to as "boggy"). (See 'Clinical presentation' above and 'Pelvic examination' above.)
●Imaging – Transvaginal ultrasound is the first-line imaging choice for evaluation of an enlarged uterus, pelvic pain, and/or abnormal bleeding. Magnetic resonance imaging is reserved for those cases in which it is important to distinguish diffuse and focal adenomyosis from leiomyomas and those cases when an accurate diagnosis is important to determine management. (See 'Imaging' above.)
●Diagnosis – Uterine adenomyosis is a histologic diagnosis made based on pathology evaluation of the uterus after hysterectomy. The diagnosis is suggested by characteristic clinical symptoms and pelvic examination, and a clinical diagnosis can be made with imaging studies. (See 'Diagnosis' above.)
●Management
•Hysterectomy – For patients with bothersome symptoms who have completed childbearing, hysterectomy is the treatment of choice. (See 'Hysterectomy' above.)
•Alternatives – For patients who have completed childbearing, uterine artery embolization (UAE) is an alternative to hysterectomy. For patients with adenomyosis who desire future pregnancy, hormonal medications may give symptomatic relief. (See 'Uterine artery embolization' above and 'Hormonal medications' above.)
•Role of uterus-sparing resection – Uterus-sparing resection of adenomyosis is an investigational approach. Patients undergoing this surgery should be counseled regarding the high rate of uterine rupture in pregnancy, most commonly remote from term, and other pregnancy complications. These patients are candidates for prelabor cesarean birth. (See 'Uterus-sparing resection' above.)
