Tom LueUnited StatesSpeakerRecent Advances in ED: Bridging Innovation and Clinical PracticeRecent Advances in ED: Translating Innovation to Patient Care
Tom F. Lue, MD, ScD(Hon), FACS, University of California, San Francisco, USA
Ischemic priapism and Peyronie’s disease are two longstanding challenges in urology. When not promptly and appropriately managed, both conditions frequently result in erectile dysfunction. This presentation will review the underlying pathophysiology of each condition and highlight recent innovations that have significantly advanced our clinical approach and improved patient outcomes.
Ischemic Priapism
Pathogenesis and Management of Ischemic Priapism
Although ischemic priapism can result from a variety of underlying conditions, they all converge on a final common pathway: paralysis of the intracavernous smooth muscle, leading to veno-occlusion and cessation of arterial inflow. This vascular stasis causes tissue ischemia, which, if not promptly reversed, progresses to necrosis, fibrosis, and ultimately erectile dysfunction.
When priapism is identified within 24 hours, initial management typically includes aspiration of the old cavernosal blood combined with intracavernosal injection of alpha-adrenergic agents such as diluted phenylephrine. These agents stimulate smooth muscle contraction, promoting restoration of venous outflow and arterial inflow.
However, once priapism extends beyond 24 hours, prolonged ischemia leads to marked tissue edema, severe smooth muscle dysfunction, and thrombosis of subtunical venules. At this stage, the efficacy of alpha-adrenergic agents is greatly diminished or absent, and surgical intervention becomes necessary. Various shunting procedures have been described to re-establish cavernosal blood flow by diverting it through the glans, corpus spongiosum, dorsal vein, or saphenous vein.
In some cases, intracavernous dilation procedures are employed to re-open the proximal-to-distal corporal channels and facilitate drainage through the shunt. These advanced measures aim to salvage erectile tissue and prevent long-term dysfunction.
Why Do Many Shunting Procedures Fail?
Within the body, exposed collagen acts as a key trigger for blood clotting. Shunting procedures create an opening in the tunica albuginea to divert blood flow toward the glans, corpus spongiosum, or the penile or saphenous veins. However, this procedure exposes collagen fibers in the tunica and surrounding injured erectile tissue, which initiates the coagulation cascade. As a result, blood clots can form within the shunt, causing its closure and leading to recurrence of priapism.
Innovation: Peri-Shunting Antithrombotic Therapy
Over the past decade, for priapism lasting more than 24 hours, we have routinely administered aspirin combined with low-dose heparin prior to shunting procedures— T-shunts, with or without intracavernous dilation. This is followed by a five-day regimen of aspirin and clopidogrel to maintain shunt patency during the critical post-ischemic hyperemia phase. Using this approach, we have effectively reduced the rate of priapism recurrence to approximately 10%.
Peyronie’s disease
Pathogenesis
Peyronie’s disease (PD) results from a complex cascade of molecular, cellular, and structural changes that cause fibrosis—with or without calcification—in the tunica albuginea, septum, or intracavernous struts of the penis. These fibrotic plaques decrease the tunica’s elasticity, leading to penile curvature, indentation, hourglass deformity, or shortening during erection. The resulting biomechanical disruption, along with the psychological distress it may cause, can contribute to erectile dysfunction.
Innovation-Enzyme-based Injection therapy
Xiaflex (collagenase clostridium histolyticum) is an enzyme-based injection therapy approved by the U.S. Food and Drug Administration (FDA) for Peyronie’s disease in December 2013. Administered via intralesional injection directly into the fibrotic plaque, Xiaflex contains enzymes that break down disorganized collagen and elastic fibers, gradually reducing and eliminating the plaque.
However, injection alone typically does not produce significant correction of the deformity without a subsequent modeling procedure. This procedure—performed manually or with devices such as RestoreX, PeniMaster Pro, or Andropenis—serves as a tissue expansion tool to promote remodeling of the normal tunica, helping to restore penile length and girth.
Over the past 11 years, the author has performed more than 11,000 Xiaflex injections and considers this approach superior to surgery for several reasons: (1) It eliminates plaques without creating new plaques, unlike surgical excision or incision with grafting; (2) It facilitates increases in penile length and girth through modeling, in contrast to the shortening often seen after plication procedures; (3) It avoids neurovascular damage and does not cause erectile dysfunction.