Keywords
pelvic reconstruction - perineal reconstruction - pelvic exenteration - VRAM - abdominoperineal
resection - flap failure
Pelvic reconstruction following abdominoperineal resection and pelvic exenteration
remains a significant challenge. Perineal wound complications occur in up to 60%[1]
[2]
[3] of patients with primary closure. The high morbidity associated with primary closure
is attributable to the large pelvic dead space, which can lead to fluid collection
and superinfection, the high tension skin closure, and the presence of irradiated
and poorly vascularized tissues.[4]
[5]
[6] The vertical rectus abdominus myocutaneous (VRAM) flap has emerged as the workhorse
flap in pelvic reconstruction, associated with significant reductions in perineal
morbidity compared to primary closure alone.[7] The advantages of flap reconstruction in this context are the obliteration of pelvic
dead space, interposition of well-vascularized tissue into an irradiated wound bed,
a decrease in closure tension, and resistance of infection.[8]
[9]
[10]
[11]
[12] Despite the purported benefits, the VRAM flap is associated with the inherent risks
of any pedicled flap reconstruction, namely, donor site morbidity and the risk of
partial or complete flap failure. The rate of complete flap loss following VRAM-based
pelvic reconstruction is less than 5%,[13]
[14]
[15]
[16]
[17] with the vast majority of failures occurring within the first 72 hours. The rates
and etiology of late flap failure, or those occurring after postoperative day 7, however,
are poorly elucidated. Herein, we propose one such mechanism of late flap failure,
occurring 13 days postoperatively due to pedicle compression secondary to bladder
distension. To the best of our knowledge, this is the first reported case of VRAM
flap loss via this mechanism.
Case Report
A 67-year-old man with a history of multiple cerebrovascular events, a myocardial
infarction, hypertension, and a 30 pack-year smoking history presented with dull 5/10
sacral pain, prompting a pelvic magnetic resonance imaging (MRI) examination. Imaging
revealed a large, well circumscribed, heterogeneously enhancing mass through the mid
body of the sacrum. Subsequent core biopsy demonstrated a sacral chordoma.
The patient underwent preoperative external beam radiation, followed by sacrectomy
and abdominoperineal resection. The colostomy was exteriorized through the left rectus
abdominus muscle. The resultant pelvic and perineal defect was reconstructed using
a right VRAM flap ([Fig. 1]).
Fig. 1 Intraoperative photograph.
The patient did well postoperatively. Following an unremarkable 5-day admission to
the intensive care unit, the patient was transferred to the orthopedic surgery unit.
Regular flap checks continued to be performed and the flap was consistently well perfused.
On postoperative day 13, the patient became systemically unwell with fever, tachycardia,
and significant abdominal discomfort. Laboratory investigations demonstrated an increase
in white blood cell count and a septic workup was initiated. During this time, the
flap demonstrated signs of both venous and arterial insufficiency ([Fig. 2]). Computed tomography of the pelvis was ordered to assess for intrapelvic collection
and revealed a markedly distended bladder with bilateral hydronephrosis. The deep
inferior epigastric pedicle could be visualized and was noted to be occluded by the
distended bladder, preventing arterial inflow and venous outflow ([Fig. 3]). The bladder was promptly decompressed, resulting in improvement in the patient's
clinical status. The perfusion to the flap, however, did not improve, ultimately resulting
in total flap loss.
Fig. 2 (A) Postoperative day 13. (B) Postoperative day 14.
Fig. 3 (A and B) Computed tomography of pelvis showing markedly distended bladder compressing VRAM
pedicle. VRAM, vertical rectus abdominus myocutaneous.
The patient was brought back to the operating room 3 weeks postoperatively for debridement
of the VRAM flap. Significant thrombosis of the deep inferior epigastric pedicle could
be appreciated in the context of a frankly necrotic flap. Following flap debridement,
bilateral advancement flaps were elevated for closure. The patient was discharged
from hospital postoperative day 40 and the wound was completely healed by postoperative
day 60.
Discussion
Flap failure in either free or pedicled flap reconstruction typically occurs within
the first 72 hours. This is often the result of intrinsic pedicle thrombosis (arterial
or venous) or extrinsic compression, eventually leading to thrombosis. In the immediate
postoperative period, traction or kinking of the pedicle is the most likely culprit
for flap failure. The incidence of and mechanisms for late flap failure, however,
remain poorly understood. The described case demonstrates clearly that pedicle compression
from a distended bladder is a potential mechanism for late flap failure and should
be considered on the differential when assessing a flap with clinical signs of vascular
compromise. Furthermore, it illustrates the utility of cross-sectional imaging in
helping to elucidate the mechanisms of late flap failure due to pedicle compression.
