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Joshi et al. Plast Aesthet Res 2022;9:22 https://dx.doi.org/10.20517/2347-9264.2021.98 Page 3 of 10

1. Over mobilization of distal urethra during anastomotic urethroplasty.

2. Presence of hypospadias and associated lack of retrograde blood supply.

3. Extensive spongiofibrosis resulting from multiple previous surgeries.

How can this happen? To perform the anastomotic urethroplasty, a dissection and mobilization of the distal
urethra is required. To mobilize the distal segment of bulbar urethra, the lateral circumflex vessels must be
sacrificed, as well as most of the perforating vessels from the cavernosa arteries. When the bulbar urethra is
transected, at the site of injury, the bulbourethral arteries also are sacrificed to reach the proximal urethral
stump and the perineal diaphragm. After transection and mobilization, the distal segment of the urethra
depends on the retrograde blood supply from the dorsal penile vessels. Thus, patients presenting with
inadequate retrograde blood supply, due to compromised dorsal penile vessels or hypospadias, might
develop BUIN.

In patients who do not present congenital vascular malformations of the blood supply of the genitals (e.g.,
hypospadias), there are two main reasons for an inadequate retrograde blood supply: (1) It is usually a result
of surgery due to the iatrogenic injury of one or both the dorsal penile artery at the time of inferior
pubectomy. Indeed, when surgeons approach the pubic bones after crura separation, the excessive use of
diathermy, especially on transverse and circumferential fashion, as well as the missed step of periosteum
[8]
elevation, may increase the risk of vascular injury and subsequently of BUIN . (2) Very rarely, as a result of
primary trauma, there can be bilateral pubic bone fractures, causing damage to either the internal pudendal
or the dorsal vessels on both sides. Such patients may develop BUIN even without iatrogenic injury. In our
large experience of over 1700 cases of PFUI treated with anastomotic urethroplasty, we reported trauma-
related vascular deficiency in only three patients, who subsequently developed BUIN. To predict this
possibility, we recommend assessing preoperatively the blood supply of the urethra with the color doppler
of the cavernosa and dorsal penile arteries. This assessment can guide surgeons during their dissection of
the posterior urethral stump, preserving the side where the dorsal penile artery showed a better flow and
deepening the dissection on the side with decreased flow.

Awareness of this pathophysiology helps prevent BUIN and its sequelae.

Incidence of BUIN
The exact incidence of BUIN is unknown. Between 1995 and 2021, we treated and managed more than 1700
patients with PFUI. Our success rate at catheter removal for primary anastomosis is 85.4% and for redo
cases is 79.1%. Of all patients treated for PFUI, 177 (approximately 9%) had BUIN. The majority of patients
[9]
with BUIN reported two or more prior failed attempts of PFUI repair . Unfortunately, the incidence of
BUIN is rising in recent years, as witnessed by a rising number of flap reconstructions (e.g., pedicle
preputial tube). Indeed, the last treatment resource for BUIN is to replace the missing urethral segment with
a vascularized flap, which can be tubularized and allows urethral continuity. Table 1 to support this
statement show that the number of flaps raised from 3-4 per year during 2010-2015 to more than 15 per
year between 2019 and 2021, with 29 flaps in the last 12 months in our units.

Evaluation of patients with BUIN
As previously described, the etiology of BUIN is an inadequate blood supply, especially the retrograde blood
supply, from the dorsal penile arteries. This inadequate blood supply is more frequently due to an iatrogenic
injury of these vessels while performing the anastomotic urethroplasty; more rarely, the deficiency is related