Grayscale Ultrasonography of Penile Corporal Fibrosis

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madman

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INTRODUCTION

Ultrasonography (US) is the primary imaging modality used for patients with penile conditions such as erectile dysfunction (ED), Peyronie’s disease (PD), penile trauma, and priapism. While patients are typically given a preliminary diagnosis based on history and physical examination, imaging is often required to confirm the diagnosis or to assess the extent of the condition. Ultrasound and magnetic resonance imaging are mostly used, but other techniques such as retrograde urethrography and computed tomography are performed in indicated cases. Currently, penile duplex Doppler ultrasonography (PDDU) is the gold standard for evaluating the etiology of ED based on hemodynamic parameters. Alternatively, standard grayscale US imaging is used to scan for non-vascular abnormalities such as fibrosis, plaques, or tunica albuginea (TA) defects.

Penile fibrosis, particularly the formation of plaques of the TA in patients with PD, has been well-studied1 ; however, the fibrosis of the corpora cavernosa is a highly prevalent sequela of various etiologies. Corporal fibrosis results from the loss of smooth muscle cells and the increase of collagen deposition. In fact, the composition of cavernosal tissue changes physiologically with age. In men between ages 41 and 60 years old, the abundance of smooth muscle cells reduces to 40% and reduces to about 35% in men over 60.2

Cases of penile corporal fibrosis may occur secondary to the explantation of an infected penile prosthesis, severe penile trauma, refractory low-flow priapism, PD, or chronic intra-cavernous injection of vasoactive drugs.3−8 Other etiologies of penile corporal fibrosis, presenting primarily with ED, can develop in chronic smokers, hypertensive patients, alcoholics, diabetics, and after radical prostatectomy.1,9,10 Corporal erectile tissue fibrosis is a significant pathophysiologic component of ED; however, current US-based penile imaging protocols do not directly assess it.


In this article, we review the literature to determine if grayscale US is a suitable imaging modality to identify and assess penile corporal erectile tissue fibrosis.




*Examination Technique

*Normal Anatomy

*Inflatable Penile Prosthesis

*Ischemic Priapism

*Penile Trauma

*Intracavernosal Injections

*Diabetes

*Peyronie’s Disease

*Vascular Disease




Discussion


We encourage providers to spend extra time to perform grayscale US, which can potentially identify and localize penile fibrosis and provide prognostic value. US should not be used to solely assess penile hemodynamics to assess ED but should also aim to capture tissue heterogeneity. In addition, grayscale US can provide an additional metric of tracking pre-and post-treatment fibrotic changes.

While grayscale US may become a valuable tool to assess corporal fibrosis, one limitation is the individual expertise required to perform and analyze US findings, a summary of which is provided in Table 1. Recognition of subtle sonographic changes is highly subjective, and normal features may be misinterpreted as fibrosis. The ultrasonographer must be knowledgeable of penile anatomy and the changes that occur due to pathological conditions. This limitation is exemplified by the number of cases of corporal fibrosis surprisingly found during penile implant surgery.85 Data remains limited in the published literature about whether these intraoperative complications occur in the absence of positive US findings. However, this could be added as a limitation to the use of grayscale US for tracking pre-operative fibrosis, as the technique is considered operator-dependent and requires both technical skill and detailed sonographic knowledge of penile anatomy.





CONCLUSION

Overall, grayscale US may be a useful and convenient imaging modality to assess penile corporal fibrosis secondary to the explantation of an infected penile prosthesis, priapism, penile trauma, chronic intra-cavernous injection of vasoactive drugs, diabetes, PD, and vascular disease. While limited by the skill and knowledge of the US operator, the combined knowledge of pathophysiology and US may help clinicians identify and manage the underlying etiology of penile corporal fibrosis.
 

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*Corporal erectile tissue fibrosis is a significant pathophysiologic component of ED; however, current US-based penile imaging protocols do not directly assess it
 
Intracavernosal Injections

Approximately 1 out of 3 men have ED that is refractory to oral phosphodiesterase-5 inhibitors, warranting treatment with intracavernosal injections (ICI) and/or other second-line agents.57,58 Compared with oral medications, ICI has a known time of onset, making them a desirable option. However, ICI involves self-injection, which is a deterrent for some patients. To administer an ICI, the user self-injects medication into their corpora cavernosa. The medication subsequently causes corporal smooth muscle relaxation, leading to an erection.59 Papaverine and prostaglandin E-1 are some of the most commonly used ICI medications.60

Most of the penile fibrosis associated with ICI comes from their potentially severe sequela. On rare occasions, ICI can cause low-flow priapism. In fact, some estimate that 5% of patients who inject themselves with papaverine develop ischemic priapism.61 The risk is significantly smaller with papaverine and prostaglandin E-1 injections.62 ICI may also act as a means of admitting bacteria into sterile penile tissue, leading to cavernositis.63 Additionally, as ICI causes minor bleeding following injection, proper post-injection pressure is needed to prevent hematoma formation.64 Low-flow priapism, cavernositis, and hematomas are all significant risks for penile fibrosis. Lastly, the repetitive microtrauma itself from injecting into the corpora cavernosa may cause fibrosis.65 To this point, some studies suggest that the most common cause of post-traumatic cavernosal fibrosis is repeated ICI usage.45,66,67

When fibrosis occurs following ICI-induced cavernositis and/ or low-flow priapism, diffuse cavernosal fibrosis may be seen on US.33,65
Fibrosis from repeated ICI use microtrauma appears on US as circumscribed, heterogeneously echogenic nodules within the corpora.33,45 These circumscribed nodules are especially common in frequent users of ICI and those who develop hematomas from improper post-injection pressure.33 Furthermore, for reasons still unknown, some patients who utilize ICI develop distal, segmental penile fibrosis that may be visualized on US.68
 
Figure 1. Normal penile anatomy displayed by transverse ultrasonography image shows the corpora cavernosa and the corpora spongiosum (*). The cavernosal arteries are identified by the curved arrows, the dorsal vessels are identified by the solid arrows, and the tunica albuginea is identified by the arrowheads. (Image used with permission from Radiographic Society of North America: Bertoloto M, et al. RadioGraphics 2009;29:477−493.
Screenshot (6896).png
 
Figure 2. Long-standing ischemic priapism displayed by longitudinal ultrasonography (left) and transverse (right) images. The arrow identifies echogenic, distorted cavernosa reflecting significant corporal fibrosis. Image has been modified from the original source and used with permission: Halls JE, et al. Br J Radiol. 2012;85 Spec No 1(Spec Iss 1): S79-S85.
Screenshot (6897).png
 
Figure 3. Circumscribed fibrosis secondary to high-flow priapism (a) Transverse ultrasonography displays bilateral cavernous hematomas (*) at the base of the penis (b) 6 months later, transverse ultrasonography displays inhomogeneity of corpora cavernosa due to fibrotic changes (*) Image used with permission from the Radiological Society of North America: Bertoloto M, et al. RadioGraphics 2003;23:495−503.
Screenshot (6898).png
 
Have you seen a paper that covers the actual treatment for penile fibrosis beyond treatments for PD?

The use of stem cells piques interest.

*Despite the amount of research on stem cells and penile fibrosis, the field is still in its infancy and is subject to many limitations. Most preclinical research regarding stem cells in penile fibrosis has focused on corpora cavernosa fibrosis owing to its clear pathophysiology (iatrogenic postprostatectomy ED and corpora cavernosa fibrosis) and representative animal models

• Owing to the complex network of cell types and interactions involved in fibrosis, very few effective medical treatment options are currently available for patients with fibrotic diseases, including penile fibrosis
 
Have you seen a paper that covers the actual treatment for penile fibrosis beyond treatments for PD?
Just extrapolating here but the only thing I could think would apply might be some type of localized steroid treatment. But haven't seen anything in the literature using that specifically.

Stem cells, as madman mentioned, would be holy grail.
 
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