Case Introduction

A 39-year-old male with a history of nephrolithiasis and gastroesophageal reflux disease presented to the urology clinic with 6 months of worsening urinary urgency, frequency and sensation of incomplete emptying. He emigrated from Russia at a young age and is a nonsmoker with an active lifestyle. Initial evaluation revealed a normal physical exam, including normal prostate exam without nodules, normal urine studies and normal serum studies including creatinine. Initial office bladder scan was notable for a post-void urinary residual of 130 cc. A trial of behavioral modification and alpha-blockade with tamsulosin was instituted, with no improvement in lower urinary tract symptoms or post-void residual. For these reasons, an office cystoscopy was recommended. Cystoscopy revealed complete absence of urinary residual, and significant distortion and extrinsic compression of the left lateral bladder wall.

Findings

Based on the cystoscopy findings, a multiphase cross-sectional computerized tomography scan was obtained, which revealed a large left pelvic arteriovenous malformation (AVM) with mass effect on the bladder (fig. 1). The AVM derived its arterial supply from the anterior division of the left internal iliac artery. The patient was referred to interventional radiology and underwent a combined percutaneous arterial and venous embolization with an Amplatzer™ vascular plug, metal coils and sclerotherapy (fig. 2). The patient experienced complete resolution of his urinary symptoms.

Teaching Point

Pelvic AVMs are rare vascular malformations characterized by multiple large abnormal communications between the arterial and venous systems, without the usual capillary interface. In contrast, the arteriovenous fistula that is more commonly seen by urologists after renal surgeries results from a single connection between the arterial and venous systems. The pathogenesis of an AVM includes enlargement of the feeding artery over time, with compensatory enlargement of the draining veins; in some cases, arterial steal syndromes, venous hypertension and high-output cardiac failure can result. AVMs are sometimes acquired from neoplastic or traumatic processes, but more commonly are congenital in nature. AVMs tend to have accelerated growth at puberty and during pregnancy, and growth occurs from enlargement of vascular structures, rather than cellular proliferation.¹

Figure 1. CT coronal reformat of the abdomen and pelvis showing a large left pelvic AVM. It is deriving arterial supply from the left internal iliac artery, draining via multiple venous varices, and demonstrates significant mass effect on the left bladder.

Figure 2. Angiographic images from Interventional Radiology showing A, high-flow vascular malformation with downstream venous aneurysm; B, embolization of the inflow tract using amplatzer plug, bentson wire and metal coils; C, post-embolization images revealing cessation of inflow without non-target embolization.

Symptoms caused by AVMs depend on the location and surrounding anatomy. Pelvic AVMs have been previously described as a rare cause of lower urinary tract symptoms and pelvic pain in men.² Cross-sectional imaging can suggest the diagnosis, but selective pelvic angiography is then required to confirm the diagnosis and ultimately treat the lesion. The goal of treatment is to occlude the nidus of the malformation. Simple surgical ligation of the feeding arterial vessel is considered ineffective, as collaterals often form, and the malformation will persist.³

Surgical removal by resection of the entire malformation can be performed when AVMs are localized and accessible, or when the AVM is large enough to mandate debulking. However, with advances in interventional radiology techniques, the minimally invasive approach has become the mainstay of treatment, especially for AVMs in the pelvis, which are relatively difficult to approach surgically. Transarterial embolization with metal coils, vinyl particles, absorbable materials or combinations thereof remains the standard of care for symptomatic patients.¹ The most feared complication of this procedure is nontarget embolization, and care must be taken to avoid inadvertent ischemia of the colon, bladder and other pelvic viscera. An alternative treatment option, which was performed in our case, is combined arterial and venous embolization. Occlusion of the draining venous outflow in addition to arterial embolization removes the venous low-pressure sump, which is thought to allow for increased collateral growth after arterial-only embolization.⁴