Endovascular management of pelvic congestion syndrome in males: A report of 2 cases

Abstract

Pelvic congestion syndrome is a well-recognized cause of chronic pelvic pain in women, but it remains underdiagnosed and rarely reported in men. Distinguishing male pelvic venous disorders from pain related to varicocele may be challenging because clinical features and imaging findings often overlap, particularly when pelvic venous reflux does not involve the pampiniform plexus. We describe 2 male patients with chronic pelvic pain in whom non-invasive imaging excluded pampiniform plexus dilation and reflux, while selective venography demonstrated abnormal venous drainage involving the paravesical, paraprostatic, pudendal, lumbar or contralateral pelvic venous plexuses. Both patients underwent targeted endovascular treatment, consisting of balloon-assisted foam embolization or vascular plug occlusion, selected according to venous hemodynamic. Each patient experienced complete and durable symptom resolution during follow-up. These cases highlight that pelvic congestion syndrome in men can appear independently of varicocele and may emerge after previous spermatic vein surgery. Recognition of this condition requires high clinical suspicion and selective venography, and tailored endovascular therapy can provide effective and sustained relief.

Introduction

Pelvic congestion syndrome (PCS) has traditionally been recognized as a cause of chronic pelvic pain in women. However, its occurrence in males is underreported and frequently underdiagnosed. While varicocele—dilation of the pampiniform plexus—is the most prevalent male pelvic venous disorder, there is increasing awareness that venous insufficiency can affect other pelvic venous plexuses within the broader spectrum of pelvic venous disorders (PeVD). Recent classification systems, such as the Symptoms-Varices-Pathophysiology (SVP) instrument, clarify these distinctions by delineating specific venous segments, thereby reducing terminological confusion [[1], [2]].

PCS is defined as chronic pelvic pain lasting more than 6 months due to pelvic venous hypertension and reflux [3]. The pathophysiology is multifaceted, involving valvular anomalies, outflow obstruction, and functional abnormalities [[4], [5]]. In men, PCS typically presents as a dull ache in the scrotum, lower abdomen, or perineum, with pain that may radiate to the thighs or buttocks and worsen with standing or physical activity. However, unlike typical varicocele, venous congestion confined to the pelvic plexuses without pampiniform involvement is difficult to diagnose and often overlooked [[6], [7], [8]].

Imaging is crucial for this distinction. While ultrasound is the first-line tool for scrotal reflux, and CT or MRI provide anatomical mapping, transcatheter venography remains the gold standard for visualizing deep reflux patterns and guiding embolization [[9], [10]]. Current literature often conflates male PCS with varicocele, leaving non-scrotal presentations poorly defined.

In this report, we present 2 unique cases of male PCS characterized by purely pelvic hemodynamic redistribution following remote varicocelectomy. Unlike standard presentations, the pampiniform plexus was competent; instead, fluid-dynamic venography revealed that symptom recurrence was driven entirely by collateralization through internal iliac vein tributaries (eg, prostatic or vesical plexuses). We aim to define this specific subset of male PCS, demonstrating that pelvic pain can persist through alternative iliac pathways even after gonadal axis obliteration, and highlighting the role of fluid-dynamic venography in guiding targeted embolization.

Case 1

A 65-year-old male presented with chronic pelvic pain persisting for 5 years, exacerbated by prolonged standing and sexual intercourse, with a Numerical Pain Rating Scale (NPRS) score of 8. His medical history included varicocele ligation at the age of 25, appendectomy, and well-controlled mild hypertension. The patient reported failure of previous pain control approaches, including neuromodulation and physical exercise.

As the pelvic pain was suggestive of persistent varicocele, the initial examination aimed to rule out its persistence or recurrence. Doppler ultrasonography showed no evidence of pampiniform plexus dilatation or reflux, even during the Valsalva manoeuvre. Considering the persistent symptoms and negative ultrasound findings, venographic study was deemed appropriate.

In the angiography suite, the right basilic vein was accessed under ultrasound guidance and a 5-French (5F) introducer sheath (Radiofocus Introducer II, Terumo, Elkton, USA) was placed. Using a 5F, 100 cm Bern angiographic catheter (Imager II, Boston Scientific, Marlborough, USA), catheterizations of left renal vein, left and right internal spermatic veins were performed. Venography was performed with Iomeprolo 350 mg/mL (Iomeron, Bracco, Milan, Italy), which confirmed the absence of reflux and ectasia in both the left and right spermatic veins.

Selective catheterization of the left internal iliac vein revealed paravesical, paraprostatic, and pudendal plexus varicose ectasia with reflux and contralateral filling on the Valsalva maneuver (Fig. 1). No significant pelvic plexus enlargement or reflux was noted on the right side at venographic study. Based on these findings, a diagnosis of PCS was established. Fluid dynamic venographic study revealed stasis of contrast performing venography via a catheter balloon (Ultraverse 035, BD, Tempe, USA). The patient underwent scleroembolization using the "Occluding-Balloon” technique via a 10 mm x 40 mm balloon catheter and instillation of 2 mL of 3% polidocanol foam (Atossisclerol, Gloria Med Pharma, Monteggio, Italy), prepared using the Tessari method, to fill the ectatic plexus only [11]. Post-procedural venography demonstrated successful scleroembolization of the dilated pelvic plexus, with no evidence of reflux or residual dilatation (Figs. 2A and B). Already at the 30-day follow-up, the patient reported almost complete resolution of symptoms, with an NPRS score of 2. At the 6-month and 12-month follow-up assessment, the patient continued to experience complete and sustained resolution of his pelvic pain symptoms. There was no increase or decrease in his NPRS score, indicating that the improvement achieved following endovascular management was maintained throughout the follow-up period.

Fig. 1.

This angiographic image demonstrates selective pelvic venography with opacification of multiple dilated and tortuous pelvic venous plexuses, consistent with pelvic venous congestion. The paravesical venous plexus (VVP) is prominently enlarged, showing irregular caliber and contrast pooling. Additional varicose ectasia involves the parasacral pelvic venous plexus (PSVP) and the pudendal/periprostatic venous plexus (PVP), which exhibit a complex plexiform appearance with serpiginous collateral channels. Within the imaged field, no opacification or dilatation of the gonadal (spermatic) veins is observed.

Fig. 2.

(A) Intra-procedural pelvic venography during balloon-occluded scleroembolization. A 10 mm × 40 mm semicompliant balloon catheter is inflated within the left internal iliac vein to hemodynamically isolate the target territory (dashed arrow). Contrast medium injected distal to the balloon demonstrates marked stasis and selectively opacifies the ectatic pelvic venous plexus adjacent to the urinary bladder (solid arrow). This creates a closed system for controlled sclerosant delivery while minimizing reflux. (B) Completion venography. Post-treatment imaging after sclerosant injection and 10 min waiting time shows the disappearance of the varicose plexus and resolution of contrast stasis within the treated territory (dotted oval). The absence of residual dilatation or reflux indicates technical success.

Case 2

31-year-old male with a history of left varicocele, previously treated with spermatic vein ligation 7 years prior, presented with pelvic and lumbar pain and a sensation of heaviness, with an NPRS score of 7. Doppler ultrasonography revealed no varicose dilation of the pampiniform plexus nor reflux signs.

Spinal pain etiologies, including intervertebral disc herniation, were already ruled out following comprehensive diagnostic workup with MRI.

Considering the possibility of varicocele recurrence and masquerading imaging phenomenon, venography was planned.

Left renal venography did not show any collateral venous vessels connecting with the testicular plexus. Venography of the proximal left spermatic vein demonstrated proximal patency without evidence of reflux to the pampiniform plexus as per distal occlusion of the vein. However, collateral vessels originating from the mid portion of the left internal spermatic vein and communicating with the lumbar vein plexus, the contralateral side, and the paravesical region were observed (Fig. 3). These findings enabled differentiation from a varicocele and suggested a diagnosis of pelvic congestion syndrome (PCS).

Fig. 3.

Sequential digital subtraction venography of the left renal–gonadal venous axis. The proximal left internal spermatic (gonadal) vein appears patent and, with distal occlusion, no reflux toward the pampiniform plexus is demonstrated within the acquired field. Despite the absence of direct collateral drainage to the testicular plexus, opacification reveals collateral outflow arising from the mid-portion of the left internal spermatic vein, with communications toward the lumbar venous plexus (LVP arrow) and across the midline to the contralateral venous system. Additional collateral drainage extends caudally toward the paravesical venous plexus (VVP arrow), outlining an alternative pelvic venous pathway potentially contributing to pelvic venous congestion.

Fluid dynamic venographic study performed with occlusion-balloon catheter technique revealed fast reflux prompting to avoid the use of liquid embolic agents. Given the risk of liquid embolic agent migration and not target embolization, a 12 mm x 9 mm vascular plug (Amplatzer Vascular Plug II, Abbott, St. Paul, USA) was selected as the preferred embolic agent. A subsequent venographic inspection confirmed successful occlusion, showing no opacification of the distal collateral segments of the internal spermatic vein (Figs. 4A and B).

Fig. 4.

(A) Venographic image demonstrating extensive collateral venous drainage originating from the mid-portion of the left internal spermatic vein (ISV). Clear opacification of these collateral vessels is observed, establishing communication with the lumbar venous plexus (LVP arrow) and the paravesical venous plexus (VVP arrows), supporting the decision to avoid liquid embolic agents because of potential non-target migration. (B) Control venography after embolization with a vascular plug shows effective occlusion of the treated segment, with no residual opacification of the distal collateral branches (dashed oval), confirming technical success.

At 30 days follow-up, the patient reported NPRS 2 to 3 with no recurrence of pelvic heaviness. No late complications were noted. A remote follow-up was conducted via telephone interview at 6 months and 18 months post-procedure confirming the persistence of the clinical benefit. The NPRS scores remained consistent with post-procedural values.

Discussion

Pelvic congestion syndrome (PCS) in males remains a rarely described condition, often overshadowed by the more commonly recognized varicocele in clinical and radiological literature. While varicocele involves dilation of the pampiniform plexus with reflux in the testicular venous system, pelvic venous disorders (PeVDs) encompass a wider spectrum, involving also pelvic venous plexuses and drainage pathways. The distinction between these entities has historically been unclear, contributing to diagnostic uncertainty and under-reporting of PCS in men.

The introduction of structured classification systems, such as the Symptoms-Varices-Pathophysiology (SVP) framework, has refined the approach to pelvic venous pathology by codifying symptoms, anatomical involvement, and reflux characteristics. In the present cases, the profile matched the pattern S2b, V2, P (L IIV, R, NT), which corresponds to chronic pelvic pain of venous origin, non-saphenous leg pain, pelvic origin, reflux linked to the left internal iliac vein, and new target reflux pathways. This phenotype highlights that chronic pelvic pain in men may present without pampiniform plexus involvement, yet with symptoms overlapping those of varicocele [12].

Clinically, the SVP classification guided a tailored interventional strategy. By pinpointing non-spermatic reflux sources (P domain)—ranging from internal iliac tributaries to perivertebral collaterals—it shifted the focus away from the gonadal axis. This anatomical targeting dictated the use of specific embolic agents (eg, sclerosants, plugs) effectively aimed at occluding these complex cross-communications.

The observed temporal relationship between chronic pelvic pain and prior varicocele ligation, occurring years or even decades later in both patients, raises the possibility that PCS in men might, in some instances, represent a secondary manifestation following venous intervention. While a direct causal link cannot be established based on this limited observational series, we hypothesize that the correction of spermatic venous reflux could potentially alter pelvic hemodynamic rather than providing a definitive resolution of venous insufficiency.

This perspective suggests a potential pathological continuum where the relief of spermatic hypertension might lead to hemodynamic shifts that, over time, could facilitate redistribution and venous overload across alternative intrapelvic venous territories. This observation is intended to be hypothesis-generating, proposing a mechanism of "secondary PCS" similar to that recognized in the literature arising from acquired factors [[13], [14]]. However, larger cohort studies are required to confirm whether prior varicocelectomy is a true risk factor for this specific pattern of recurrence.

Our cases demonstrate that male PCS is not strictly dependent on pampiniform plexus failure. The hemodynamic redistribution we observed highlights the pivotal role of the internal iliac pathways. Crucially, the documented reflux in our cases exclusively involved the paravesical, paraprostatic, pudendal, and lumbar venous plexuses, bypassing the testicular veins entirely. The necessity of selective venography to confirm this non-pampiniform venous reflux underscores the diagnostic limitations of non-invasive modalities like Doppler ultrasound, which may miss deep pelvic venous abnormalities.

Clinically, the pain features of male PCS, a dull heaviness worsened by standing or exertion, are often indistinguishable from those of varicocele. Therefore, recognizing that these persistent or recurrent symptoms can result from collateral venous hypertension should broaden the diagnostic scope for men following varicocele treatment.

A rigorous differential diagnosis is essential, as male PCS shares overlapping symptoms with several non-vascular conditions. Primary exclusions include Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS), which typically presents with lower urinary tract symptoms (LUTS), ejaculatory pain, or prostatic tenderness [15]; and pelvic floor muscle dysfunction, characterized by muscle hypertonicity or dyssynergia impacting voiding or defecation [16]. In our cases, the absence of LUTS, sexual dysfunction, or palpable muscle tenderness on physical examination rendered these etiologies unlikely. Furthermore, Pudendal Neuralgia was excluded based on the nature of the pain. While pudendal neuralgia typically manifests as neuropathic pain (burning, electric shock) aggravated by sitting (Nantes criteria) [17], our patients reported dull, gravitative pain exacerbated by prolonged standing and physical exertion—a hallmark of venous congestion. Ultimately, the exclusion of these clinical mimics, combined with the selective venographic demonstration of pathological reflux, confirmed the diagnosis of male PCS.

Endovascular embolization proved effective in both cases, providing durable symptom relief and supporting its role as a safe and definitive treatment option. The use of different embolic strategies, as liquid sclerosant and vascular plugs, demonstrates the necessity of tailoring therapy to the anatomical reflux pattern to achieve optimal results and minimize non-target embolization and is supported by robust literature [[18], [19]].

Several limitations of this report must be acknowledged. First, clinical success was assessed primarily using the Numerical Pain Rating Scale (NPRS). While useful for tracking symptom intensity, this subjective measure represents a limitation as it fails to capture the broader functional impairment and quality-of-life changes associated with chronic pelvic pain. The absence of validated, multidimensional instruments restricts a more comprehensive evaluation of patient outcomes.

Furthermore, the retrospective nature of this report precluded a standardized follow-up protocol. Follow-up duration was heterogeneous (30 days, 6-month and 12 month and 30-days, 6-months and 18-months, respectively) and relatively short to mid-term. Specifically, objective anatomical verification via post-treatment imaging was not routinely performed. This reflects current clinical practice, where repeat catheter venography is considered unjustified in patients with symptom resolution due to radiation exposure and invasiveness. Similarly, non-invasive cross-sectional imaging (CT/MRI) is limited by supine positioning, which may fail to detect dynamic, gravity-dependent reflux or residual venous dilation. Consequently, long-term anatomical stability implies a speculative assumption based on clinical symptom maintenance rather than radiological evidence. Looking forward, the integration of AI-assisted imaging and computational 3D dynamic modelling—similar to approaches used in neurovascular systems—could help address the sensitivity limitations of conventional CT and MRI. These technologies could be adapted to simulate pelvic venous flow redistribution following spermatic vein ligation, offering predictive insights into the hemodynamic mechanisms proposed in this report [20]. Moreover, while explainable AI frameworks could help predict hemodynamic patterns, the complexity of chronic pelvic pain demands attention to the interplay between vascular congestion and neuromuscular function. Recent electromyographic evidence has demonstrated that pelvic venous congestion can induce persistent pelvic floor muscle hypertonicity which may not immediately normalize despite effective embolization [21]. Therefore, future protocols should evaluate central mediators of vascular tone and consider adjunctive therapies—such as biofeedback and stress reduction—to maximize outcomes in patients with long-standing neuromuscular adaptation."

In summary, these cases demonstrate that PCS in men, though rare and challenging to diagnose, should be recognized as a distinct entity within the spectrum of PeVDs. The adoption of modern classification systems enables more precise differentiation from varicocele and may reshape understanding of long-term outcomes following varicocele repair. Ultimately, these insights expand awareness of new venous pathways of pain generation in men, emphasizing the importance of vigilant follow-up and consideration of pelvic venous plexus involvement in patients with unexplained chronic pelvic pain.

Declaration of generative AI and AI-assisted technologies in the writing process

The authors declare that no generative AI or AI-assisted technologies were used in the preparation of this manuscript.

Ethical approval

The study was conducted in accordance with the Helsinki Declaration of 1975 (as revised in 1983) and institutional ethical standards. The privacy rights of human subjects were respected throughout the study and manuscript preparation.

Author contributions

All authors contributed to the conception of the work, data collection, image analysis, interpretation of findings, drafting and critical revision of the manuscript. All authors approved the final version of the manuscript.

Patient consent

Written informed consent for publication of clinical details and diagnostic images was obtained from both patients prior to submission. The consent documents are retained by the authors and will be provided to the journal upon request in exceptional circumstances. Patient privacy has been protected by removing all identifying information from the manuscript and images.