A 95-year-old man presented with progressive right lower extremity swelling. He reports a chronic history of overflow incontinence. Laboratory evaluation revealed a normal coagulation profile, creatinine of 1.5 milligrams per deciliter. A venous duplex ultrasound demonstrated acute occlusive deep venous thrombosis (DVT) in the right lower extremity. A computed tomography (CT) venogram confirmed acute DVT extending from the distal external iliac veins to the superficial femoral veins bilaterally, and an enlarged urinary bladder with a massive right-sided diverticulum measuring 12.7 by 6.4 centimeters compressing the external iliac veins bilaterally (Figure 1). A CT pulmonary arteriogram showed right lower lobe subsegmental pulmonary emboli (PE).
The cause of the DVT was thought likely due to compression of his external iliac veins from an enlarged bladder diverticulum. A heparin drip was started, and a Foley catheter was placed for decompression of the urinary bladder. The patient remained hemodynamically stable with improving right lower extremity swelling and bladder emptying. He was discharged on apixaban for PE, tamsulosin for suspected benign prostatic hyperplasia (BPH), and a Foley catheter with follow-up for further workup of his urinary obstruction.
Discussion:
First-time venous thromboemboli (VTE) have a significant effect on morbidity and mortality, and healthcare costs. Cancer, surgery, and immobility have been thoroughly studied and found to be associated with development of VTEs. However, the presentation of a DVT provoked by a large bladder diverticulum has rarely been described. There are few case reports of similar iliac vein thrombi from external compression in the form of uterine leiomyomas, psoas abscesses, and hip synovial cysts.
The pathophysiology involves a series of events that leads to venous stasis. The first insult is the development of a bladder diverticulum, which can be acquired from urinary outflow obstruction due to BPH, cancer, external sphincter dysfunction, and urinary stasis from a neurogenic bladder. There can also be points of weakness in the bladder detrusor muscle that allows for bladder mucosal herniation. Afterwards, there is extrinsic compression of the iliocaval veins increasing the risk for DVTs.
Management may include anticoagulation, transfemoral thrombectomy and iliac vein stenting, and removing the source of compression. In terms of a bladder diverticulum, it is usually resolved with relief of the outlet obstruction, such as placement of a Foley catheter. Diverticulectomy is a surgical option. Since this case represents the patient’s first VTE and was provoked by a temporary risk factor, “stasis,” the recommended length of anticoagulation is three to twelve months.
Conclusions:
Our case emphasizes the role of “stasis” as a risk factor for VTEs. This is especially important because the sources of external compression may be easily treated, preventing recurrence of VTEs and limiting the duration of anticoagulation.