In March 2020, Gül et al first described hard-flaccid syndrome (HFS) in the medical literature with a presentation of 4 cases.¹ Despite only receiving attention recently in the literature, patients have been self-diagnosing themselves and finding support for this condition in online forums for over a decade.² HFS represents a diagnostic dilemma due to unfamiliarity among many urologists and lack of an evidence-based definition. Patient’s often have a sense of despair and hopelessness as their complaints are disregarded or attributed to other diagnoses. We hope this article will help raise awareness of HFS among the urology community.

HFS is a symptom cluster accompanied by penile sensation changes, a semi-rigid phallus during the flaccid state, decreased morning/nocturnal erections, decreased erectile rigidity, difficulty maintaining erections, pain with ejaculation and pain with urination.² Not all symptoms are necessary, but no formal diagnostic criteria exist. However, a semi-rigid phallus, penile sensation changes and erectile dysfunction (ED) are the most common findings. Urinary symptoms appear to be related to pelvic floor dysfunction and muscle tightness. Men are commonly in their 20s and 30s and often have comorbid anxiety and/or depression. HFS is an acquired condition that follows a traumatic event to the base of an erect penis. Most reported cases to date report trauma during sexual intercourse or aggressive masturbation.^1,3

Although the exact mechanism of HFS remains to be determined, it is thought to result from injury to the pudendal nerve and artery.¹ HFS has a wide range of symptoms involving all aspects of the male sexual cycle; there seems to be a plausible element of autonomic neuropathy with exaggerated sympathetic stimulation in response to urogenital trauma resulting in loss of coordinated neurovascular response to sexual stimuli. Potentially, there could be overlap with other conditions such as chronic pelvic pain syndrome, the male counterpart to female persistent genital arousal disorder (PGAD)/genito-pelvic dysesthesia (GPD) or a penile entity of complex regional pain syndrome (see figure). However, pain is necessary for the diagnosis of chronic pelvic pain syndrome, and most patients with HFS do not report pain.²

Figure 1. Overlap of HFS, pain syndromes and sexual arousal disorders.

The diagnosis of HFS is made based largely on history and physical exam. Men with HFS often complain of a cold or numb sensation to the penis, but especially the glans. Physical exam is typically unimpressive but often notable for a partial engorgement during the flaccid state. Some men have tenderness along the corpora. Hormonal evaluation in all reported cases has been unremarkable. Further, radiologic studies including penile ultrasound and pelvic magnetic resonance imaging have not revealed any abnormalities.¹

Just as HFS can be challenging to identify and diagnose, the treatment is equally frustrating for providers and patients. Given the lack of reports in the literature, there is no standardized treatment. Phosphodiesterase-5 inhibitors, especially daily tadalafil, appear to be the most common treatment. Varying results have been reported, with most reports showing the benefit is diminished when the medication is discontinued. Others have also suggested benefit from pelvic floor physical therapy (PFPT) and relaxation techniques.

In the original series by Gül et al, 1 patient was treated with low-intensity shock wave therapy (Li-SWT) with initial improvement. Based on this early report, we have subsequently treated 3 men at our institution with Li-SWT. These patients underwent 6 treatments in which shocks were delivered to the left, right, ventral and dorsal aspects of the stretched penis. The scrotum was lifted, and additional shocks were administered to the right and left crura. All patients tolerated the treatments well with no pain. All patients began to notice improvement after the third treatment in regards to the engorgement of their penis during the flaccid state. Following 6 treatments, 1 patient reported complete resolution of all symptoms (ED, pain and partial penile engorgement). The other 2 men noted initial improvement in hardness of the flaccid penis. Our results are encouraging, although the durability of Li-SWT remains to be determined. Further work is needed to identify if any adjunct therapies such as daily tadalafil or PFPT provide additional benefit in combination with Li-SWT.

HFS is as real as ED, PGAD/GPD and postorgasmic illness syndrome. It represents a needed area of future research to establish an evidence-based definition, diagnostic criteria and treatment. There is history of genitourinary trauma in most patients with a wide range of symptoms involving all aspects of the male sexual cycle. It is also a great diagnostic challenge with unremarkable laboratory findings and imaging in most patients. It appears that the trauma results in autonomic neuropathy with sympathetic overdrive and loss of coordinated neurovascular response to sexual stimuli. We can draw parallels from existing literature on female PGAD/GPD with significant overlap with HFS; it is plausible HFS could be the male PGAD/GPD. Optimal treatment remains to be determined but daily tadalafil, PFPT and Li-SWT appear promising.