What is the differential diagnosis for a patient with acute pelvic pain?
What causes of pelvic pain require inpatient admission?
What causes of pelvic pain require surgical management?
A 27-y.o. gravida 1 para 1 presents to the emergency room with 4 hours of crampy pain in the right lower quadrant. She has intermittent nausea, and her last menstrual period was 3 weeks ago. Her urine pregnancy test is negative, and her pelvic exam is notable only for mild right adnexal tenderness.
Acute pelvic pain is an exceedingly common complaint. In the most recent, nationally representative data from Emergency Department (ED) use in the United States, the most common reason for an emergency room visit by females aged 15 to 64 years old (5.5 million visits) was for abdominal pain, cramps, or spasms. This was also the most common complaint in female patients aged 65 years and older.1 This chapter will review the general approach to the ED patient with pelvic pain, followed by details on individual gynecologic conditions that may present with pelvic pain. The diagnosis and management of ectopic pregnancy is discussed in Chapter 54.
The list of conditions that may present with pelvic pain is intimidatingly long and includes diagnoses associated with significant morbidity and mortality risks (Table 55-1). The close proximity of the female pelvic organs and their visceral innervations mean that vague, poorly localized and/or referred pain is often present. The first step in the assessment is to determine the stability of the patient, and if she proves unstable, to help ED staff determine the interventions necessary to stabilize her condition. This may include the recognition of a surgical emergency, such as a ruptured ectopic pregnancy, followed by immediate surgical intervention. More commonly, however, the patient is stable, and it is best to start with a full, broad differential diagnosis.
TABLE 55-1Differential Diagnosis of Acute Pelvic Pain ||Download (.pdf) TABLE 55-1 Differential Diagnosis of Acute Pelvic Pain
|Gynecologic Causes ||Nongynecologic Causes |
Ruptured/hemorrhagic ovarian cyst
Pelvic inflammatory disease
Ovarian hyperstimulation syndrome
Septic pelvic thrombophlebitis
Pelvic floor spasm/tension myalgia
Vaginal or vulvar trauma
Bowel obstruction, perforation, or ischemia
Inflammatory bowel disease
Benign bowel pain (e.g. constipation) Urinary retention, inflammation, or infection
The history of present illness, risk factors, review of systems, and abdominal and pelvic examination make each item on the differential more or less likely, narrowing and focusing the differential to a manageable level and guiding laboratory and imaging workup. It is particularly useful to figure out early in the encounter whether the pain is truly acute, as opposed to an exacerbation of chronic pelvic pain, because the latter can lead to an entirely different differential diagnosis. Box 55-1 lists the diagnostic process when presented with a patient with acute pelvic pain.
Box 55-1 Initial Approach to Diagnosing a Patient with Acute Pelvic Pain
Assess the overall stability of the patient.
Assess whether the patient requires surgical intervention.
Perform a pregnancy test to rule out obstetric etiologies.
Differentiate between acute pain etiologies and exacerbation of chronic pain.
Differentiate between gynecologic and nongynecologic etiologies.
Ovarian cysts are fluid-filled structures that can form as part of a physiologic or pathologic process. Such cysts are considered simple if completely anechoic upon ultrasound. A simple cyst of < 3 cm diameter in a reproductive-aged woman is considered an ovarian follicle, and this finding is completely normal. Cysts with internal septae, solid components, or both are considered complex.
Physiologic ovarian follicles and cysts form as part of the cyclic ovulatory process. However, luteal cysts can persist or enlarge; the levonorgestrel intrauterine device (IUD) can increase the risk of luteal cyst persistence. While ovarian cysts can be normal, cyst rupture can cause acute pelvic pain and is often suspected when free fluid is found in the posterior cul-de-sac.
The differential diagnosis of ovarian cysts includes luteal cysts, hemorrhagic cysts, endometriomas, dermoid cysts, peritoneal inclusion cysts, paratubal cysts, hydrosalpinx, and malignant adnexal masses. A patient with acute pain in the setting of an ovarian cyst should be evaluated for ovarian torsion, which is discussed in the following section. Other causes of pain due to ovarian cysts include a ruptured cyst, distension of tubal tissue, mass effect from a large cyst, and complications of malignancy.
While most ovarian cysts are benign, patients should be evaluated for their risk of malignancy. The most important risk factors for ovarian cancer are age and a family history of ovarian, breast, or colon cancer; BRCA mutations and Lynch syndrome also carry significant risks of ovarian malignancy.
Acute onset of pain with peritoneal signs can signal rupture of an ovarian cyst. Mass effect from a cyst can lead to sensations of pelvic pressure and frequent urination. Complaints of dysmenorrhea, dyschezia, and dyspareunia may be associated with endometriosis and endometrioma. Concerning symptoms of malignancy include weight changes, bloating, early satiety, increased abdominal girth, and abnormal uterine bleeding or postmenopausal bleeding, which can occur secondary to increased estrogen levels associated with sex-cord stromal tumors.2
A complete abdominal and pelvic exam should be performed. Peritoneal signs may be present if rupture has led to peritoneal irritation. A large cyst may be palpable upon bimanual exam. Evaluation of groin lymph nodes should be done as well, especially if suspicion for malignancy exists.
Anemia may be demonstrated on a complete blood count (CBC) if a ruptured cyst results in hemorrhage. While screening tests for ovarian malignancy are lacking, serum testing for CA 125 and other serum tumor marker panel tests can help guide decisions for referral to a gynecologic oncologist. CA 125 is nonspecific and can be elevated with various disease processes, including endometriosis, PID, or cirrhosis. Newer tumor marker panels include the multivariate index assay (MIA), which evaluates CA 125, prealbumin, apolipoprotein A-1, β2-microglobulin, and transferrin, or the Risk of Malignancy Algorithm (ROMA), which considers human epididymis protein 4, CA 125, and menopausal status.24
Transvaginal ultrasound (TVUS) is the preferred modality for imaging the adnexa and any adnexal masses or cysts. Most cysts have a classic ultrasound finding that can aid in identification. Hemorrhagic cysts have a fine reticular or netlike pattern. Endometriomas are characterized by homogeneous, low-level echoes in the absence of a solid component. Dermoid or mature teratomas are likely to contain hyperechoic nodules, fluid levels, and calcifications. Cyst rupture may lead to a collection of free fluid in the posterior cul-de-sac, but this finding is nonspecific, as women of reproductive age have been found to have physiologic-free fluid in the pelvis, independent of any pathologic process. Reassuring ultrasonographic characteristics associated with benign cysts include thin-walled, simple cysts and the absence of complex findings such as solid components, thick septations, or evidence of Doppler blood flow. Additional concerning ultrasound findings include ascites or a fixed mass. Abdominal computed tomography (CT) is utilized to identify metastases.
Primary management for ovarian cysts is conservative. Even in the case of a ruptured hemorrhagic cyst, bleeding and pain are usually self-limited. Pain can be managed with nonsteroidal anti-inflammatory drugs (NSAIDs). However, if vital sign instability is noted or heavy or persistent blood loss is suspected, surgical management may be indicated.
Simple cysts are usually benign and can be closely observed with serial ultrasounds if they are < 10 cm. Many cysts, even those containing complex components, will resolve spontaneously; a study involving 6807 women with abnormal cysts were followed with ultrasound, and 63.2% of them resolved spontaneously.3 Another study found that 69.4% of postmenopausal women with unilocular cysts < 10 cm had spontaneous resolution, and no cases of cancer were diagnosed over a 6-year period of follow-up.4 While a definitive size cutoff has not been established, a cyst > 10 cm is typically treated with surgical removal.
In premenopausal patients, an ovarian cystectomy can be performed with care not to disrupt the blood supply to the ovary. In perimenopausal or postmenopausal patients, the risks and benefits of oophorectomy should be discussed. In addition, each patient's individual risk of cancer should always be considered while making treatment decisions, and surgery by a gynecologist oncologist should be recommended if there is concern for a malignant process.
Patients with known ovarian cysts undergoing conservative management should be given torsion precautions. Cyst progression or resolution can be monitored with serial ultrasounds.
Adnexal torsion refers to the pathologic twisting of the ovary, fallopian tube, or both, causing partial or total occlusion of its blood supply.
Adnexal torsion can occur when the ovary, fallopian tube, or both become unbalanced around the axis created by the infundibulopelvic and utero-ovarian vessels. Although studies conflict on the diameter of ovaries most likely to cause torsion, and torsion may occur with either normal adnexa or adnexal mass, very small and very large ovaries are unlikely to torse. This is presumably because very small ovaries are relatively well balanced around their vascular axis, and very large ovaries lack the space needed to twist. However, torsion can and does occur in premenarchal girls, and the frequency of torsion occurring with normal adnexa is higher in this age group. Dermoid cysts may be more likely to unbalance the adnexa, probably because of the large difference in density between their primarily fatty content and normal ovarian tissue. Torsion of the right ovary is more common than of the left; the tendency for right-sided torsion is attributed to a longer right-sided utero-ovarian ligament and the prevention of torsion on the left due to the bulk of the sigmoid colon.
There is no set of diagnostic criteria that can accurately predict the presence or absence of torsion, and negative findings at the time of surgery for suspected torsion are common. However, there are risk factors that, if present, can raise the level of suspicion (Table 55-2). The history should include if a preceding activity led to onset of pain, as vigorous activity including intercourse can be the inciting event. Other risk factors include a history of cysts or torsion, polycystic ovarian syndrome (PCOS), ovarian stimulation, and pregnancy.
TABLE 55-2Findings Associated with Adnexal Torsion ||Download (.pdf) TABLE 55-2 Findings Associated with Adnexal Torsion
|Finding ||Percentage of Patients with Torsion |
|Acute onset pain ||90–100 |
|Right-sided pain ||60 |
|Nausea ||70 |
|Vomiting ||45 |
|Fever ||20 |
|Unilateral tenderness ||70 |
|Palpable adnexal mass ||25 |
|Mild leukocytosis ||27–50 |
|Abnormal adnexal structures on ultrasound ||Unknown |
|Absent ovarian vein flow on color Doppler ||40 |
By far, the most consistent symptom caused by adnexal torsion is acute onset, unilateral pelvic pain. In the majority of cases, this pain is accompanied by nausea, and often by vomiting as well. Pain that is affected by position changes, such as lying down or leaning forward, is also suggestive.
Findings from physical examination are inconsistent. A significant minority of patients will have a low-grade fever. An enlarged, tender adnexa is suggestive, but pelvic exam findings range from completely normal to showing peritoneal signs.
An important step in the laboratory evaluation of patients with the above described presentation is a pregnancy test to rule out ectopic pregnancy. Laboratory findings are otherwise typically normal, although mild leukocytosis is not uncommon.
The cornerstone of evaluation for adnexal torsion is pelvic ultrasound with assessment of color Doppler flow to bilateral adnexa. This method classically shows an enlarged, heterogeneous, edematous ovary because the lymphatic drainage and venous flow are affected before arterial perfusion. The absence of flow has a high positive predictive value for torsion, but the converse is not true, as up to 60% of torsion patients have positive Doppler flow.5
A patient who is suspected to have intermittent torsion that has resolved may be offered outpatient follow-up if she is clinically stable. Precautions should be given to the patient, and she should be instructed to seek immediate care if symptoms of torsion return.
Surgical treatment is required for suspected ovarian torsion, as viability of the ovarian tissue requires detorsion. A cystectomy should be performed concurrently, if applicable, because rates of recurrent torsion are high if the adnexa is simply detorsed or if the cyst is merely drained. Detorsion of black-and-bluish-appearing adnexa allows resumption of viable function in most cases, and salpingo-oophorectomy generally is not required. A study of 58 ischemic-appearing adnexa reported that 54 patients showed follicular ovarian development upon follow-up ultrasound.6 Ovarian necrosis can occur without detorsion, which results in reduced fertility and a nidus for infection. If the patient has a history of recurrent torsion, oopexy can be considered.
PELVIC INFLAMMATORY DISEASE
Pelvic inflammatory disease (PID) is a spectrum of conditions characterized by inflammation and infection of the upper female reproductive tract. Any combination of endometritis, salpingitis, tubo-ovarian abscess (TOA), and pelvic peritonitis may be present.
The overall incidence of PID in the United States has decreased over the past decades. Data reported by the Centers for Disease Control and Prevention (CDC) from 2005 to 2014 demonstrates a decrease in PID of 71% among women aged 15 to 44 years in all geographic areas. Despite this decrease, PID still accounts for 51,000 outpatient visits per year and is the primary diagnosis in 6.4% of all inpatient gynecologic hospitalizations.7
The lower genital tract is home to a unique microbiological environment containing pathological and nonpathological bacteria coexisting in a constantly fluctuating balance. This nonsterile environment is separated from the sterile upper genital tract by the endocervical canal, which provides an architectural defense and contains cervical mucus, which is usually impermeable to ascending bacteria. Infection with sexually transmitted bacteria (most commonly Neisseria gonorrhoeae and Chlamydia trachomatis) can breach the standard defenses of the endocervical canal. The fall of this barrier allows entry to the upper genital tract by lower genital flora, resulting in varying combinations of endometritis, salpingitis, TOAs, and pelvic peritonitis. Therefore while PID is most commonly precipitated by one of these sexually transmitted pathogens, the upper-genital-tract infection itself is generally considered to be polymicrobial.
Because of the wide spectrum of symptomatology, from asymptomatic to septic, PID is notoriously difficult to characterize by diagnostic criteria. The CDC recommends against the use of diagnostic criteria; empiric treatment for PID is suggested for all women with abdominal or pelvic pain, and either cervical motion tenderness, uterine tenderness or adnexal tenderness without an other diagnostic explanation for their pain, and either cervical motion tenderness, uterine tenderness or adnexal tenderness.8
Risk factors for the development of PID include young age, multiple sex partners, history of prior PID or sexually transmitted infection, and history of sexually transmitted infection in a previous or current partner. Given the serious sequelae of infertility and chronic pelvic pain that can result from untreated PID, a low threshold for this diagnosis is necessary when evaluating a patient with pelvic pain, especially with the above risk factors. Box 55-2 lists the features associated with an increased likelihood of PID.
Box 55-2 Factors Increasing the Likelihood of a Diagnosis of PID
Oral temperature of > 38.3°C
Abnormal cervical mucopurulent discharge or cervical friability
Presence of abundant numbers of white blood cells on saline microscopy of vaginal fluid
Elevated erythrocyte sedimentation rate
Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis
Although the presence of one or more of these factors increases the specificity of the diagnostic criteria, treatment for PID should be provided to any sexually active woman with cervical motion tenderness or adnexal tenderness or uterine tenderness.
Reproduced with permission from Workowski KA, Bolan GA; Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines, 2015, MMWR Recomm Rep. 2015 Jun 5;64(RR-03):1-137.
As discussed previously, symptoms in PID may be nonspecific, mild, or even absent. A directed review of symptoms may reveal dyspareunia, intermenstrual or postcoital bleeding, or abnormal vaginal discharge. The pain associated with PID is usually bilateral and mild to moderate. Severe, unilateral pain may be present in PID complicated by a TOA.
As already mentioned, in any sexually active woman, just one of the following is required to meet the minimum criteria for PID diagnosis: cervical motion tenderness, uterine tenderness, or adnexal tenderness. Other exam findings that may be present (but are not necessary for diagnosis) include fever, abnormal cervical or vaginal discharge, and cervical friability.
No specific laboratory findings are associated with PID. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) levels may be elevated, but this finding is nonspecific. A leukocytosis may be present, but it is usually only notable in severe cases. Documentation of bacterial pathogens (including gonorrhea or chlamydia) by culture or nucleic acid amplification is sometimes possible, but it is not a necessary criteria for diagnosis.
Similarly, the diagnosis of PID does not depend on any specific imaging findings; however, some key findings may be of assistance. A pelvic ultrasound or MRI may demonstrate thickened, fluid-filled fallopian tubes or a tubo-ovarian complex, although most patients without TOAs will have normal imaging. Classically, TOAs will appear as complex, multilocular masses and may contain internal echoes consistent with inflammatory disease.
Patients with PID can be triaged to inpatient or outpatient treatment based on clinical criteria. Recommended criteria for inpatient admission include failed outpatient treatment, pregnancy, noncompliance, inability to tolerate oral medications due to nausea or vomiting, severe clinical illness (high fever or severe abdominal pain), or pelvic abscess. In patients who do not meet the criteria for inpatient treatment, outpatient treatment has been shown to have comparable efficacy and long-term results.9
The goal of antibiotic therapy in PID is to provide broad-spectrum coverage for a presumptively polymicrobial infection, including coverage for N. gonorrhoeae and C. trachomatis. Standard treatment regimens are presented in Table 55-3. It should be noted that patients with an IUD in place do not need to have the device removed upon diagnosis of PID unless they fail to make clinical improvement in 48 to 72 hours.
TABLE 55-3Treatment Regimens for PID
Patients should be instructed to abstain from intercourse until therapy is completed for herself and her sexual partner. Patients should be encouraged to discuss their diagnosis with their partners to ensure that the other person or persons receive adequate treatment as well. Patients should be reminded of the importance of completing the entire 14-day course of treatment. Given the association of PID with high-risk sexual behavior, patients should be tested for other sexually transmitted infections, including human immunodeficiency virus (HIV) and syphilis. History of PID is a risk factor for recurrence, with 1 in 4 women experiencing disease recurrence.10 Therefore patients should be counseled about modifiable risk factors for disease recurrence and methods of prevention. Patients with recurrent PID are 1.8 times more likely to suffer from infertility and are 4.2 times more likely to experience chronic pelvic pain.11
An infected fluid collection in the pelvis can arise as a result of a postsurgical or postprocedural complication, complicated PID, diverticulitis, appendicitis, or an inflammatory bowel disease such as Crohn's disease. By definition, a postsurgical pelvic abscess involves the organs or spaces that were manipulated during a surgery and meets at least one of the following criteria:12
Purulent drainage from a drain that is placed through a stab wound into the organ/space
Organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space
An abscess or other evidence of infection involving the organ/space that is found upon direct examination, during reoperation, or via histopathologic or radiologic examination
Pathogenic microorganisms from the skin, vagina, and cervix can infect the surgical site, resulting in vaginal cuff cellulitis, pelvic cellulitis, and pelvic abscesses. Risk factors include infection prior to surgery, postoperative hematoma, and long surgical duration. Gynecologic procedures are typically polymicrobial and involve more than the aerobic, Gram-positive cocci typical of skin bacteria. Endogenous vaginal flora is comprised of both pathogenic and nonpathogenic bacteria of facultative and obligate anaerobic Gram-positive or Gram-negative species; thus gynecologic surgical site infections can include Gram-negative bacilli, Enterococci, group B Streptococci, and anaerobes.13 In one study examining transgluteal percutaneous drainage of pelvic abscess, laboratory cultures were positive in 90% of patients and Escherichia coli was the most prevalent microorganism, found in 77.8% of the positive samples.14
Superficial surgical site infections should be differentiated from deeper abscesses. Superficial infections, under which vaginal cuff cellulitis is included, are characterized by pain, purulent discharge, localized swelling, warmth, or erythema. These findings may or may not overlay a deeper abscess.
Pelvic abscesses typically prevent with pain and fever. Postsurgical pelvic abscesses may present a week or more after surgery.
Findings upon examination occur over a wide range, from only mild local tenderness to sepsis with fever, tachycardia, and tachypnea.
Laboratory workup in the setting of a pelvic abscess is nonspecific, with markers of inflammation present, including leukocytosis, and elevated ESR and CRP.
CT with both intravenous (IV) and oral contrast is the imaging modality of choice when abscess is suspected. It shows a defined cystic mass with peripheral rim enhancement.
Regardless of the plan for surgical or percutaneous drainage, antibiotics should be initiated immediately upon diagnosis of a pelvic abscess. It can be difficult to determine the source of the abscess, and a polymicrobial process involving gut and/or genitourinary flora should be assumed, and coverage selected appropriately. If complicated PID is a possibility with the differential diagnosis, either doxycycline or IV clindamycin should be a component of the regimen (as in the PID regimens, discussed previously) so that coverage for C. trachomatis is provided.
Large abscesses will likely require percutaneous drainage by interventional radiology, or transvaginal, laparoscopic or open drainage in the operating room. While it is unclear what specific size would require drainage, a review of 122 TOA patients found that all the abscesses < 2 cm responded to antibiotics alone. The mean TOA size that responded to antibiotics was 4.4 cm, and the mean size requiring surgery was 7.3 cm. All patients who had an abscess measuring > 10 cm required drainage.15 Failure to treat an abscess adequately can lead to sepsis or breakdown of a vaginal cuff repair or abdominal incision.
Patients with pelvic abscesses are managed similarly to those with severe or complicated PID. A transition to oral antibiotics is generally made after 24 to 48 hours of clinical improvement, and treatment continued for at least 14 days. When possible, antibiotic selection should be guided by culture results from the drainage procedure. Any drains are left in place until drainage is minimal and nonpurulent.
Intraabdominal inflammation and subsequent adhesion formation can lead to complicated future pelvic surgery; patients with a history of pelvic abscess should be counseled with regard to increased complication risks.
Uterine fibroids are benign tumors resulting from the overgrowth of smooth muscle cells within the myometrium. They are classified as subserosal, intramural, or submucosal, according to their location relative to the endometrial cavity and uterine wall (Fig. 55-1). Fibroid degeneration occurs when a fibroid outgrows its blood supply, leading to ischemia, necrosis, and pain.
Classification of leiomyomas. (Reproduced with permission from Hoffman BL, Schorge JO, Bradshaw KD, et al: Williams Gynecology, 3rd ed. New York, NY: McGraw-Hill; 2016.)
Fibroids are the most common female pelvic tumor, but their true incidence is difficult to estimate, given that most studies are conducted on women with symptoms or who have had a hysterectomy. Race is a major risk factor for the development of fibroids, with black women having an almost threefold age-specific cumulative incidence compared to white women.16 Fibroids are hormonally responsive, so they typically shrink and are less likely to cause new symptoms after menopause.
The pathophysiology of fibroid growth is poorly understood but consists of two primary steps. First, a normal myocyte is transformed into an abnormal myocyte. Second, this abnormal myocyte undergoes a monoclonal expansion, becoming a clinically relevant tumor. While fibroids are benign uterine tumors, malignancy must remain part of the differential diagnosis for any uterine mass, and there is no reliable way to differentiate a benign myoma from a malignant leiomyosarcoma preoperatively.
Fibroids are often asymptomatic, but when they cause pain, it is usually due to the pressure that they place on adjacent organs, and a slowly evolving, chronic discomfort occurs. Complications of fibroids that can present as acute pelvic pain include degeneration or necrosis, acute urinary retention, prolapse or vaginal expulsion, and torsion of a pedunculated fibroid.
Uterine fibroids, although very common, rarely cause acute pain complications, and therefore the diagnosis is often one of exclusion.
Pain secondary to fibroid degeneration usually arises over days to weeks. Acute onset of pain can point to a rarer, more acute complication. Pain symptoms for patients with fibroids may be associated with symptoms of heavy or abnormal uterine bleeding.
Degenerating fibroids are typically tender to palpation and may be associated with a low-grade fever. An enlarged uterus with an irregular contour may be palpable on exam. A prolapsing fibroid may be identified as a cervical or vaginal mass.
TVUS is the first-line modality for imaging the pelvic organs, and it also can demonstrate the presence and location of fibroids. A degenerating fibroid may be painful when pressure is exerted on the fibroid by an ultrasound probe. For additional delineation of fibroid location or surgical mapping, pelvic magnetic resonance imaging (MRI) may be useful. Gadolinum contrast can be used to identify areas of degeneration, as degenerated portions of fibroids show no enhancement. If urinary retention due to fibroids is the cause of pain, an enlarged bladder may be seen with either imaging modality.
Conservative management is an option if an asymptomatic fibroid is incidentally found. However, in a patient presenting with pain secondary to fibroids, the primary options are medical and surgical. Medical management includes oral contraceptive pills, medroxyprogestone acetate, leuprolide acetate, or a levonorgestrel IUD. The first-line therapy for pain secondary to degenerating fibroids involves the use of NSAIDs, sometimes requiring admission for pain control with IV ketorolac. Additional options available in some centers include uterine artery embolization (UAE), myolysis, and ultrasound or MRI-guided radiofrequency ablation (RFA) of fibroids. Surgical removal of fibroids can be done by myomectomy or hysterectomy. As with any surgery for pelvic pain, patients must be counseled that fibroid resection may not alleviate their pain completely.
Pain from fibroid degeneration is a self-limited process, typically lasting 2 to 4 weeks. However, patients remain at risk for further pain episodes if other fibroids are present. Following myomectomy, the 5-year recurrence rate for fibroids requiring subsequent surgery is estimated to be approximately 9%.17 This rate depends on the number of fibroids removed initially, with a higher recurrence risk for patients with multiple fibroids removed. The definitive treatment for uterine fibroids is hysterectomy, and patients should be counseled regarding this option if more conservative management attempts fail.
Hematometra is defined as distension of the uterus with blood or fluid, and is caused by obstruction within the uterine cavity or cervix. Hematocolpos is distension of the vagina with blood or fluid, and is caused by a more distal obstruction of the genital tract. With accumulation of fluid, this may progress to hematometrocolpos, or distension of the uterus and vagina with blood or fluid.
Hematometra rates due to reproductive tract anomalies are difficult to track, given the low frequency of anomalies in the general population. Imperforate hymen is more common than transverse vaginal septum, with an estimated prevalence of 0.5 per 1000 women.18 Transverse vaginal septum is estimated to occur in only 1 in 30,000 to 1 in 80,000 women.19
Hematometra can be caused by any disease that results in a physical obstruction of the flow of blood or fluid from the uterus through the cervix. The three main etiologies are uterine anomalies, cervical stenosis due to prior surgery or malignancy, and obstruction from uterine synechiae, known as Asherman syndrome. While there are several possible causes of hematometra, reproductive tract anomalies are the primary cause of hematocolpos and hematometrocolpos. Anomalies associated with hematocolpos and hematometrocolpos include imperforate hymen, transverse vaginal septum, obstructed hemivagina, and vaginal agenesis.
Patient age and procedural history are essential components of distinguishing the underlying etiology of hematometra. In an adolescent with primary amenorrhea and cyclic pain, a reproductive tract anomaly is the most likely cause. Alternatively, in an older patient with history of uterine curettage or ablation, uterine adhesions are more likely.
Patients typically present with acute but cyclic pain, with timing mimicking a menstrual cycle, associated with primary or secondary amenorrhea.
Upon examination, patients with hematocolpos will have evidence of a reproductive tract anomaly, such as an imperforate hymen or vaginal septum, often with bluish tint. Hematometra will cause uterine enlargement and tenderness, and may cause enough distension that an abdominal mass is palpable.
Ultrasound (whether transabdominal or transvaginal) will reveal a distended, fluid-filled uterus, vagina, or both. If the etiology is Asherman syndrome, pockets of echogenic fluid may be seen rather than a single, large fluid collection. MRI can be performed to evaluate further if a complex reproductive tract anomaly is suspected based on ultrasound or surgical findings.
The mode of treatment for hematometra is dependent on the specific etiology, but the underlying goal is relief of the obstruction. If the hematometra is the result of an obstructive anatomical anomaly like an imperforate hymen or transverse vaginal septum, the treatment is surgical. One technique to relieve the obstruction is to create a series of incisions in a stellate pattern through the obstructing tissue, and then use a running, absorbable suture along the tissue edges to create patency and allow the passage to heal.
If the hematometra is secondary to cervical stenosis, cervical dilation will relieve the obstruction and allow the outflow of fluid. Hysteroscopic resection of intrauterine adhesions may be necessary if the obstruction is in the lower uterine segment or more superior uterine body. In the appropriate clinical setting, an endocervical curettage can be used to exclude malignancy as the source of the obstruction. If purulent material is encountered, cultures should be sent and the patient should be treated with broad-spectrum antibiotics.
For prevention of recurrence of hematometra due to cervical stenosis, a pediatric Foley catheter can be sewn into place in the cervical canal and left for a period of 10 to 14 days. The patient should be treated with prophylactic antibiotics during this time. An alternative therapy includes weekly dilations until patency is achieved. For both cervical stenosis and uterine synechiae, if the obstruction cannot be permanently relieved or if the patient experiences recurrent pain or infection, definitive treatment with a hysterectomy may be indicated.
OVARIAN HYPERSTIMULATION SYNDROME
Ovarian hyperstimulation syndrome (OHSS) is a condition that can occur following ovulation induction as part of an assisted reproductive technology (ART).20 It is a potentially lethal condition, and 3% to 8% of in vitro fertilization cycles are complicated by moderate or severe OHSS. OHSS is an exaggerated response to exogenous gonadotropin stimulation characterized by enlarged ovaries and third spacing, especially into the abdominal cavity, and is associated with bloating, an increased risk for venous thromboembolism (VTE) and decreased organ perfusion.21
Increased intravascular permeability occurs secondary to increased levels of human chorionic gonadotropin (hCG) and vascular endothelial growth factor (VEGF). Increased levels of renin in the ovarian follicular fluid and angiotensin have also been implicated in the development of OHSS. Used for luteal phase support in ART cycles, hCG upregulates the production of VEGF receptors and VEGF, a potent stimulator of the vascular endothelium. Third spacing results as fluid shifts from the intravascular space, primarily into the abdominal cavity.25
Risk factors for developing OHSS with ART include young age, low body weight, PCOS, use of high-dose exogenous gonadotropins, high serum estradiol level, high number of ovarian follicles, successful pregnancy following ART, and history of OHSS.22
OHSS is typically suspected based on a history of recent iatrogenic ovarian stimulation. Criteria for the diagnosis of mild, moderate, severe, and critical OHSS are shown in Table 55-4. If OHSS is suspected, the patient should be concurrently evaluated for thrombosis, as there can be a 4.1% incidence of VTE in severe cases.23
TABLE 55-4Classifications of OHSS and Associated Symptoms ||Download (.pdf) TABLE 55-4 Classifications of OHSS and Associated Symptoms
Abdominal distension or discomfort
Mild nausea or vomiting
No laboratory abnormalities
|Features of mild disease and |
Ultrasonographic evidence of ascites
Elevated hematocrit (> 41%)
Elevated white blood cell count (> 15,000)
|Features of moderate disease and |
Oliguria or anuria
Greater than 2-pound weight gain in 24 hours
Severe abdominal pain
Hematocrit > 55%
White blood cell count > 25,000
Serum creatinine > 1.6 mg/dL
Creatinine clearance < 50 mL/min
Hyponatremia < 135 mEq/L
Abnormal liver function tests
|Worsening of the abovementioned criteria, including |
OHSS is a self-limiting condition that typically resolves after a few days. Most mild and moderate cases can be managed on an outpatient basis. The treatment is conservative and directed at relieving symptoms. Oral analgesics and precautionary counseling should be provided to patients. Intercourse and strenuous activity may increase the risk of ovarian rupture or torsion, and should be avoided.22 If symptoms worsen, daily physical examination, weight monitoring, and serial hematocrit, electrolytes, and creatinine should be performed.
Patients should be advised to drink at least 1 liter of fluid per day; electrolyte drinks are preferable. Hospitalization for OHSS should be considered if severe criteria are met. Inpatient care should include the following:
Frequent vital signs and strict monitoring of input and output
Measuring daily weight and abdominal circumference at the navel
Physical examination, with care to avoid bimanual exam of the ovaries
Follow-up lab tests, including CBC, electrolytes, liver function tests (LFTs), and creatinine
Ultrasound, to assess ascites and ovarian size
X-ray if pleural effusion is suspected; echocardiogram if pericardial effusion suspected
Paracentesis, if symptomatic ascites is present
Fluid resuscitation may contribute to ascites and third spacing, but correction of hypovolemia is important. To help avoid hyponatremia, 5% dextrose in normal saline is preferred over lactated ringers. If plasma expansion is necessary, albumin (25%) 50 to 100 g over 4 hours is preferred; dextran should be avoided because of its association with development of acute respiratory distress syndrome (ARDS). Diuretics are not recommended until the intravascular volume has been restored.22
Routine VTE prophylaxis is not recommended for patients undergoing ART. However, if a severe case of OHSS develops after assisted reproduction, prophylactic low-molecular-weight heparin (LMWH) is recommended by the Chest 2012 guidelines for 3 months after resolution of OHSS.22
Communication of the diagnosis to the patient's reproductive endocrinology and infertility specialist is critical to maintain an appropriate level of ongoing surveillance as well as to reduce the risk of recurrence in future cycles.
SEPTIC PELVIC THROMBOPHLEBITIS
Septic pelvic thrombophlebitis, particularly ovarian vein thrombosis (OVT), is a diagnosis of exclusion. It should be suspected in recently postpartum or postoperative gynecology patients with pelvic pain and low-grade temperature unresponsive to broad-spectrum antibiotics. Fever can occur in a spiking pattern. The diagnosis can sometimes be confirmed by a CT scan revealing a thrombus in the ovarian vein, more frequently on the right side.26
Therapeutic anticoagulation with heparin or LMWH constitutes the commonly referenced treatment, but there is little data to guide drug selection or duration of treatment. For a complete description of the epidemiology, diagnosis and management of septic pelvic thrombophlebitis, please see Chapter 44.
CASE 55-1 FOLLOW-UP
Ultrasound reveals an enlarged right ovary with a 4-cm complex cystic mass and absent flow on color Doppler. The patient is taken for urgent diagnostic laparoscopy, where right adnexal torsion is confirmed. The adnexa is detorsed, and a 4-cm dermoid cyst is removed from the right ovary. The patient is discharged home from the recovery room in good condition.
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