Chronic Pelvic Pain Attributable to Pelvic Congestion Syndrome: A Case Series

A 41-year-old woman, gravida 2 para 2 (2 full-term spontaneous vaginal deliveries), presented with CPP and left lower abdominal pain persisting for 5 years. Despite consulting multiple gynecologists and receiving continuous oral and injectable analgesics, her symptoms did not improve. She also reported intermittent chest pain over the past 3 to 4 years, with visual analogue scale (VAS) pain scores ranging from 5 to 10, with the pain particularly severe during menstruation. Over the years, she was advised to undergo hysterectomy or psychiatric evaluation, as no organic cause was identified. At her consultation in October 2020, a vascular etiology was suspected. She expressed relief that her pain was being thoroughly investigated. Transvaginal ultrasound showed an anteverted-flexed uterus without adnexal mass, while pelvic venous ultrasound revealed left pelvic vein engorgement. Pelvic radiography, sonography, and lumbar spine evaluations were unremarkable. Further imaging with IVDSA and CT in November 2020 confirmed the coexistence of Nutcracker syndrome, characterized by compression of the left renal vein between the aorta and superior mesenteric artery, and iliac vein compression consistent with May–Thurner anatomy, with compression of the left common iliac vein by the right common iliac artery. These findings were associated with reflux into the left ovarian vein and marked pelvic venous congestion ( Figures 1 and 2 ). She was formally diagnosed with pelvic congestion syndrome secondary to combined venous outflow obstruction, including Nutcracker syndrome and iliac vein compression consistent with May–Thurner anatomy. Figure 1 Computed tomography angiography (CTA) revealed compression of the left renal vein between the abdominal aorta and the superior mesenteric artery, consistent with Nutcracker Syndrome. This compression obstructed venous drainage, causing increased pressure in the left renal vein leading to collateral circulation through the left gonadal vein, resulting in its engorgement (blue arrows). The image highlights the anatomical relationship between the vessels and the surrounding structures, providing visual evidence of the condition. Computed tomography angiography showing compression of the left renal vein, consistent with Nutcracker Syndrome. Figure 2 Computed tomography angiography (CTA) image showing engorgement of the left gonadal vein due to collateral circulation (blue arrows). This CT scan image illustrates the vascular system in the abdominal area, focusing on the left gonadal vein which appears enlarged due to changes in blood flow. The image highlights the vein's engorgement, suggesting a compensatory mechanism in response to venous obstruction. This condition is often associated with pelvic congestion syndrome, where blood flow is redirected due to blockages in other veins, such as those seen in Nutcracker syndrome and May–Thurner syndrome. The image provides insight into the complex interplay of vascular structures and the body's adaptive responses to maintain circulation. CT scan reveals enlarged left gonadal vein linked to altered blood flow patterns. Computed tomography angiography (CTA) revealed compression of the left renal vein between the abdominal aorta and the superior mesenteric artery, consistent with Nutcracker Syndrome. This compression obstructed venous drainage, causing increased pressure in the left renal vein leading to collateral circulation through the left gonadal vein, resulting in its engorgement (blue arrows). Computed tomography angiography (CTA) image showing engorgement of the left gonadal vein due to collateral circulation (blue arrows). According to the SVP classification, these cases were coded as S12V12P, with obstruction of the left common iliac vein (LCIV O NT), reflux in the left gonadal vein (LGV R NT), and obstruction of the left renal vein (LRV O NT). Given the progressive symptoms and failure of conservative management, endovascular intervention was recommended. In March 2021, she underwent balloon angioplasty and kissing stenting of the bilateral iliac veins. Additionally, left renal vein angioplasty and embolization of the left ovarian vein were performed to relieve Nutcracker syndrome-related congestion ( Figure 3 ). Intraoperative imaging confirmed successful venous decompression. Postoperatively, she experienced immediate and complete pain relief, with VAS pain scores decreasing from 10 to 0. She no longer required analgesics. Follow-up imaging confirmed resolution of venous engorgement and patent stents. Over the following year, she remained symptom-free and gradually resumed normal activities, with serial evaluations confirming sustained recovery and no evidence of recurrent congestion. Long-term follow-up at 1- and 2 years post-procedure demonstrated continued symptom resolution and durable treatment outcomes. Figure 3 Intravenous digital subtraction angiography (IVDSA) revealed significant obstruction and reflux in the left iliac vein, leading to multiple collateral circulations (Right). In contrast, the left iliac vein demonstrates smooth blood flow to the heart without significant obstruction or reflux (Left). These images illustrate different conditions of the iliac vein, highlighting the presence of collateral circulations in the first image and unobstructed flow in the second. Two angiographic images showing iliac vein conditions: obstruction with reflux and smooth blood flow. Intravenous digital subtraction angiography (IVDSA) revealed significant obstruction and reflux in the left iliac vein, leading to multiple collateral circulations (Right). In contrast, the left iliac vein demonstrates smooth blood flow to the heart without significant obstruction or reflux (Left). A 41-year-old woman, gravida 2 para 2, presented with CPP and vulvodynia for 6 years, with a baseline VAS pain score of 5, increasing to 10 during menstruation. She also reported lower limb swelling for 4 years. Despite multiple consultations and a diagnosis of dysmenorrhea and adenomyosis, prolonged medical therapy with oral and injectable analgesics failed to provide relief. She eventually underwent laparoscopic subtotal hysterectomy in 2021 at another institution, but her symptoms persisted, prompting further evaluation. At her consultation in March 2022, vascular congestion was suspected as the underlying cause. Laparoscopic examination the following month revealed pelvic vein engorgement and adhesions ( Figure 4 ). Further imaging, including IVDSA and multidetector computed tomography (MDCT), confirmed IVCS and PCS ( Figure 5 ). A peripheral vascular evaluation (Viasonix system) also demonstrated possible venous compression, with both mean venous outflow (MVO) and segmental venous capacitance (SVC) values below the reference range, supporting the diagnosis. Figure 4 Laparoscopic examination revealed the left peritoneal wall with multiple engorged pelvic veins and adhesions. Two laparoscopic views of the pelvis. The upper image shows the left peritoneal wall with multiple enlarged, tortuous, engorged veins consistent with pelvic varicosities. The lower image shows laparoscopic instruments handling tissue in the same area, with adhesions and inflamed peritoneal surfaces. Laparoscopic view showing dilated pelvic veins and adhesions on the left peritoneal wall. Figure 5 Intravenous digital subtraction angiography (IVDSA) and multidetector computed tomography (MDCT) demonstrating significant obstruction and reflux in the left iliac vein with extensive collateral circulation. On IVDSA (upper panels), the red arrow indicates the site of venous obstruction, while the blue arrow highlights a dilated collateral vessel. On MDCT (lower panels), the red arrow indicates compression of the left common iliac vein, consistent with iliac vein compression syndrome. In contrast, the right iliac vein demonstrates smooth blood flow without significant obstruction or reflux. The upper left panel shows an intravenous digital subtraction angiography (IVDSA) image with a red arrow indicating the site of venous obstruction in the left iliac vein. The upper right panel displays another IVDSA image with a blue arrow highlighting a dilated collateral vessel. The lower left panel presents a multidetector computed tomography (MDCT) image showing the iliac veins and surrounding structures. The lower right panel features an MDCT image with a red arrow indicating compression of the left common iliac vein, consistent with iliac vein compression syndrome. The right iliac vein demonstrates smooth blood flow without significant obstruction or reflux. Four panels showing IVDSA and MDCT images of iliac vein obstruction and collateral circulation. Laparoscopic examination revealed the left peritoneal wall with multiple engorged pelvic veins and adhesions. Intravenous digital subtraction angiography (IVDSA) and multidetector computed tomography (MDCT) demonstrating significant obstruction and reflux in the left iliac vein with extensive collateral circulation. On IVDSA (upper panels), the red arrow indicates the site of venous obstruction, while the blue arrow highlights a dilated collateral vessel. On MDCT (lower panels), the red arrow indicates compression of the left common iliac vein, consistent with iliac vein compression syndrome. In contrast, the right iliac vein demonstrates smooth blood flow without significant obstruction or reflux. In May 2022, she was formally diagnosed with IVCS and PCS secondary to central venous outflow obstruction. According to the SVP classification, this was coded as S23V23P, with obstruction of the left common iliac vein (LCIV O NT), reflux in the left internal iliac vein (LIIV R NT), and reflux in the left gonadal vein (LGV R NT). Three weeks later she underwent balloon angioplasty and kissing stenting of the bilateral iliac veins, guided by intraoperative sonography. To further relieve venous congestion, left renal vein angioplasty and left ovarian vein embolization were performed ( Figure 6 ). The embolization was performed to address pelvic venous reflux, a key pathophysiological mechanism of pelvic congestion syndrome even in the absence of Nutcracker syndrome. Intraoperative imaging confirmed successful stent placement and venous decompression. Figure 6 Endovascular treatment with bilateral iliac vein stenting (left: left iliac vein; right: right iliac vein), performed in conjunction with left gonadal vein embolization. The images show two IVDSA views of the pelvic region. Additionally, the left gonadal vein embolization is evident, with coils visible in the left side of the image. The stents and coils are positioned to address venous congestion and reflux. The anatomical structures, including the pelvic bones and spine, are faintly visible in the background, providing context for the location of the stenting and embolization procedures. Two IVDSA images showing bilateral iliac vein stenting and left gonadal vein embolization. Endovascular treatment with bilateral iliac vein stenting (left: left iliac vein; right: right iliac vein), performed in conjunction with left gonadal vein embolization. The patient reported immediate symptom relief, with VAS pain scores decreasing from 10 to 0 within a week. Over the next few months, she experienced a 3-kg weight loss and marked improvement in lower limb swelling. At follow-up visits over the first year, she remained pain-free, with imaging showing patent stents and no evidence of recurrent venous congestion. By one-year post-procedure she had fully recovered, with resolution of pelvic pain, vulvodynia, and lower limb swelling. A 38-year-old woman, gravida 2 para 2, presented with CPP persisting for approximately 1 year, accompanied by left inguinal and sacral pain that worsened when sitting. She also reported low back pain and severe dysmenorrhea, with a VAS pain score of 10 during menstruation, requiring analgesics for symptom control. Despite multiple gynecologic consultations and treatments, her symptoms persisted. A hysterectomy was suggested at another institution, but she declined and sought further evaluation. At her initial consultation in August 2021, transvaginal ultrasound revealed a retroverted-flexed uterus and a left ovarian cyst (2.7 × 3.7 cm), and urinalysis showed occult blood. Other laboratory tests were unremarkable. Peripheral vascular ultrasound and Viasonix deep venous evaluation demonstrated mild venous insufficiency with regurgitant flow over the bilateral saphenofemoral junctions, but no evidence of deep vein thrombosis. Further imaging with IVDSA and CT in October 2021 confirmed IVCS, with compression of the left common iliac vein by the right common iliac artery, consistent with May-Thurner syndrome. According to the SVP classification, this was coded as S2V2P LCIV O NT ( Figure 7 ). Figure 7 Intravenous digital subtraction angiography (IVDSA) revealed significant obstruction and blood flow reflux in the left iliac vein, leading to the formation of multiple collateral circulations. This has led to the formation of multiple collateral circulations. The angiography highlights the vascular structures and the areas of obstruction, providing a detailed view of the affected region. The image is consistent with findings related to May-Thurner syndrome, where the left common iliac vein is compressed by the right common iliac artery. Intravenous digital subtraction angiography showing obstruction and collateral circulation in the left iliac vein. Intravenous digital subtraction angiography (IVDSA) revealed significant obstruction and blood flow reflux in the left iliac vein, leading to the formation of multiple collateral circulations. In December 2021 she underwent balloon angioplasty and kissing stenting of the bilateral iliac veins. Postoperatively, her VAS pain score decreased from 10 to 0–1, and she no longer required analgesics. At follow-up visits over the first year, she remained symptom-free, with no recurrence of pain. A vascular re-evaluation in March 2024 confirmed no significant venous outflow impairment, supporting the long-term success of the intervention.

Chronic pelvic pain (CPP) is among the oldest and most challenging conditions in medicine, with descriptions tracing back to ancient Egypt around 1550 BCE. 1 In the 19th century, French anatomists Richet (1857) and Aran (1858) first reported varicose veins in the utero-ovarian plexus as a potential cause of pelvic pain, a condition now known as pelvic congestion syndrome (PCS). This vascular mechanism was further supported by Lefevre (1964), who linked broad ligament varicocele to multiparity, and by Chidekel (1968), who demonstrated retrograde filling of the left ovarian vein on renal venography. 2 CPP remains highly prevalent, affecting an estimated 6% to 25% of reproductive-age women, and accounting for up to 10% of gynecologic outpatient visits and 40% of diagnostic laparoscopies; however, it is a symptom, not a diagnosis. 3 Its nonspecific, multifactorial nature, spanning gynecologic, urologic, gastrointestinal, and functional disorders, often results in misdiagnosis and inappropriate treatment. 4 The lack of a universally accepted definition further complicates management. The Royal College of Obstetricians & Gynaecologists (RCOG) defines CPP as intermittent or constant pain in the pelvis for ≥ 6 months, unrelated to menstruation, intercourse, or pregnancy, while the American College of Obstetricians and Gynecologists (ACOG) use slightly different thresholds and criteria. 5 Gynecologic causes of CPP include endometriosis, pelvic inflammatory disease (PID), adhesions, adenomyosis, leiomyomas, and pelvic floor dysfunction. Less common but clinically important are PCS, ovarian remnant syndrome, and gynecologic malignancy. 6 Although PCS is not a common cause of CPP, it is particularly relevant because it is a reversible cause of CPP. Classic clinical features such as post-coital ache combined with ovarian point tenderness have been reported to have a sensitivity of approximately 91% to 94% and specificity of 77% to 80% in diagnosing PCS. 7 , 8 In this case series, we describe 3 women with longstanding CPP who endured years of debilitating pain, ineffective treatments, and unnecessary surgical interventions before ultimately being diagnosed with PCS through comprehensive evaluations. These cases highlight the physical and emotional toll of delayed or missed diagnosis, as well as underscoring the importance of maintaining awareness of vascular causes of CPP. The cases demonstrate how systematic diagnostic assessment can uncover reversible etiologies, alleviate prolonged suffering, optimize management strategies, and reduce the personal and healthcare burden associated with misdiagnosis and delayed treatment.

We retrospectively reviewed medical records from 2019 to 2024 to identify patients with CPP lasting more than 6 months, in whom common gynecologic and gastro-enterologic causes had been excluded. From these records, we selected 3 representative patients with longstanding CPP who were ultimately diagnosed with PCS following comprehensive evaluations. These cases were chosen to illustrate the varied clinical presentations, prolonged symptom trajectories, and diagnostic challenges of CPP, and to underscore how systematic evaluation and recognition of vascular features can lead to the correct diagnosis and resolution of symptoms. All 3 patients underwent systematic assessment with symptom-based scoring, followed by vascular imaging, including lower limb venous ultrasound, intravenous digital subtraction angiography (IVDSA), computed tomography (CT), or magnetic resonance (MR) venography, to identify venous compression, reflux, or collateral circulation. Once PCS was confirmed, endovascular interventions were performed. All 3 patients underwent balloon angioplasty and kissing stenting of the bilateral iliac veins. This study was conducted in accordance with the ethical standards of the institutional and national research committees and with the 1964 Helsinki Declaration and its later amendments. The study protocol was reviewed and approved by the Institutional Review Board (IRB) of our institution, Taipei Municipal Wanfang Hospital (Managed by Taipei Medical University) (Approval No. [B202505042]). Written informed consent was obtained from all patients for the use of their anonymized clinical data, intraoperative findings, and postoperative outcomes for research and publication purposes.

CPP remains a common yet often misunderstood condition, with multifactorial etiologies spanning gynecologic, urologic, gastrointestinal, and musculoskeletal causes. Although PCS accounts for only a subset of CPP cases, its specific clinical and radiologic features make it an actionable diagnosis when appropriately considered. However, as seen in these cases, PCS is frequently overlooked, partly due to inconsistent definitions, overlapping symptoms with other disorders, and limited awareness among clinicians. These cases demonstrate that systematic assessment, including careful history-taking, exclusion of common etiologies, and targeted vascular imaging is crucial to uncovering treatable vascular causes of CPP. Early recognition and intervention alleviate long-term patient suffering and also reduce unnecessary procedures and healthcare utilization.

The 3 cases presented in this report provide insights into the importance of early recognition, accurate diagnosis, and appropriate management of PCS as a reversible cause of CPP secondary to venous outflow obstruction. Case 1 highlights how delayed recognition of vascular pathology can lead to prolonged suffering due to misdiagnosis as a gynecologic or psychological condition. Case 2 underscores that gynecologic surgery alone does not always address the underlying venous pathology, emphasizing the necessity of vascular assessment in patients who do not respond to surgery. Case 3 illustrates how a systematic and multidisciplinary evaluation can uncover a vascular etiology even in patients with relatively recent-onset symptoms and atypical presentation. Despite initial recommendations for hysterectomy, careful assessment revealed positional pain, venous insufficiency, and May-Thurner syndrome on imaging, highlighting the importance of considering vascular causes and avoiding unnecessary surgical interventions. These cases reinforce the need for a multidisciplinary approach to CPP, incorporating vascular evaluation in patients unresponsive to conventional treatments. PCS is thought to result from pelvic venous insufficiency and dilatation, which may be primary, due to congenital absence of valves or intrinsic venous wall weakness, or secondary, due to mechanical obstruction such as Nutcracker syndrome 9 or iliac vein compression syndrome. 10 While its detailed pathophysiology remains under investigation, recognizing PCS is critical because it represents an actionable diagnosis that is often overlooked. 11 , 12 PCS is frequently misdiagnosed and difficult to manage. PCS accounts for 10% to 20% of gynecologic consultations; however, only about 40% of cases are referred to subspecialists or specific care teams. 2 , 13 PCS is also known as known as pelvic venous insufficiency, and is due to the incompetency of the internal iliac vein, the ovarian vein, or a combination of the venous structures in the pelvis. 2 , 13 Notably, PCS is frequently the cause of CPP; around 10% of women have isolated ovarian varices and about 60% of these women have PCS. 2 , 13 The overall prevalence of PCS ranges from 6% to 27% worldwide, and is estimated to be the cause of CPP in up to 30% of women. 2 , 13 Although the etiology of PCS is unclear, it is likely multifactorial with hormones, venous insufficiency due to valves, venous obstruction, and secondary to concurrent medical conditions, such as peripheral artery disease. 2 , 13 As shown by the 3 cases presented herein, endovascular therapy is effective at treating the syndrome. CPP is a symptom that may be caused by many underlying conditions including gynecologic (eg, endometriosis, pelvic inflammatory disease, fibroids), urologic (eg, bladder pain syndrome, interstitial cystitis), gastrointestinal (eg, irritable bowel syndrome), and musculoskeletal disorders. 13–15 The initial workup for CPP should include urine analysis and blood tests to exclude pregnancy, anemia, or infection, and pelvic ultrasound should be performed to evaluate for adnexal masses, uterine abnormalities, and other pelvic pathology. 13–15 In patients with unexplained pelvic pain despite a thorough evaluation, PCS should be suspected and vascular studies should be performed. 13–15 The diagnostic evaluation of patients with suspected PCS usually begins with non-invasive Doppler ultrasound to assess pelvic vein dilatation and abnormal blood flow. 2 , 16 Doppler sonography is then followed by CT or MR venography to delineate venous anatomy, and identify the presence of venous compression and collateral circulation. 16 , 17 Invasive techniques such as intravascular ultrasound (IVUS) and catheter-based venography, considered the “gold standard” for diagnosis of PCS provide high-resolution, direct assessment of venous obstruction and its severity, and may be performed to help identify treatment options or if there is a high index of suspicion of PCS and prior non-invasive studies are negative or equivocal. 2 , 13 , 18 In addition, it is important to emphasize that endovascular or surgical treatment for PCS must be carefully planned and anatomically precise. Inadequate or inappropriate intervention may paradoxically worsen venous outflow and aggravate symptoms, as illustrated by a reported case in which iliac vein stenting across an unrecognized anomalous internal iliac vein drainage led to worsening pelvic congestion until targeted embolization was performed. 19 This underscores the necessity of comprehensive preoperative imaging and individualized treatment strategies to avoid iatrogenic exacerbation of PCS. Treatment options for PCS include conservative management and medical and interventional therapies. Conservative management includes compression stockings for lower extremity swelling, pain control with NSAIDs or neuropathic agents, and pelvic floor physical therapy with behavioral interventions. 5 Medical therapy includes the use of anticoagulants. The European Society for Vascular Surgery (ESVS) 2022 Clinical Practice Guidelines on the Management of Chronic Venous Disease of the Lower Limbs consider direct oral anticoagulants (DOACs) as the preferred anticoagulant therapy for patients with central venous outflow obstruction (CVOO) with a treatment duration of 6 to 12 months, with the latter if thrombosis is present. 20 As evidenced by the 3 cases presented herein, interventional treatments for PCS including endovascular stenting, balloon angioplasty, and embolization of incompetent pelvic veins can relieve venous hypertension and improve symptoms in up to 80% of women, and thus may be considered the preferred treatment option in patients who do not respond adequately to conservative therapy. 13 , 21 , 22 In this context, kissing stent placement may be used to optimize venous outflow and maintain symmetry at the iliocaval confluence. However, as bilateral stenting remains controversial and may introduce additional risks, this approach should be individualized based on anatomical and intraoperative findings. Although left renal vein stenting has been proposed as a treatment option for Nutcracker syndrome, its use remains controversial due to potential complications such as stent migration, thrombosis, and uncertain long-term outcomes. Therefore, patient selection should be cautious, particularly in younger individuals. In refractory or complex cases, surgical bypass or thrombectomy may be considered, particularly when thrombosis or severe obstruction is present. 22 Ovarian vein embolization targets venous reflux, a key driver of pelvic venous hypertension in PCS. Rather than simply reducing venous drainage, embolization interrupts pathological reflux pathways within the pelvic venous system. Given the extensive collateral networks of the pelvis, including deep, superficial, and gonadal pathways, alternative routes of venous return can be preserved after embolization. 23 However, in cases with significant proximal venous outflow obstruction, embolization alone may be insufficient and should be combined with interventions that restore venous patency. Therefore, treatment decisions should be individualized. In our cases, treatment decisions were guided by imaging and intraoperative findings, and interventions were performed only when hemodynamically significant abnormalities, such as venous compression or pathological reflux, were identified. This finding-based approach allows targeted treatment of clinically relevant lesions while avoiding unnecessary interventions.

This case series underscores the importance of recognizing venous outflow obstruction as an underappreciated cause of PCS and demonstrates that endovascular intervention can achieve sustained symptom relief. Patients with CPP unresponsive to conventional gynecologic treatments should undergo comprehensive vascular evaluation, particularly for IVCS and NCS. Timely diagnosis may facilitate faster recovery and avoid unnecessary procedures, whereas delayed recognition prolongs suffering and increases healthcare burden. Balloon angioplasty, venous stenting, and left ovarian vein embolization are effective, minimally invasive treatments that offer durable symptom resolution and should be considered key components of PCS management secondary to venous compression syndromes.

This case series is descriptive in nature and, as such, is not intended to establish causal relationships or treatment efficacy across broader populations. The diagnostic approach—including the selection of imaging modalities and interpretation of findings—varied slightly across cases, reflecting real-world clinical variability but potentially limiting reproducibility. Furthermore, although the follow-up duration extended up to two years, longer-term outcomes remain unknown, and recurrence beyond this period cannot be excluded. Future prospective studies using standardized diagnostic criteria and validated outcome measures are needed to further define optimal assessment strategies and confirm the long-term efficacy of vascular interventions in patients with PCS-associated CPP.