Perforator flaps frequently rely on small vessels for their supply, which may lead to problems with flap viability. To ensure a more dependable blood supply, larger perforators are sought either on preoperative imaging or intraoperatively. Body weight gain is usually associated with increasing cutaneous perforator size. The question remains whether body weight loss causes a diminution in the size of these perforators.
Sixty-seven consecutive patients were recruited, each undergoing either deep inferior epigastric perforator flap breast reconstruction (n = 57) or abdominoplasty (n = 10), with measurement of all abdominal wall deep inferior epigastric artery perforators. This was calculated with either preoperative computed tomographic angiography scans or intraoperative measurements.
Higher body mass index (>29) was associated with a 2.7-fold increase in number of 1.5-mm perforators (p < 0.01), a 1.3-fold increase in the average diameter of the five largest perforators (p < 0.01), and a 1.2-fold increase in the diameter of the largest perforator (p < 0.01). Subsequent loss of body weight did not reduce the size of perforators. Patients who had been previously heavier had an average of a 2.6- to 3.3-fold increase in the number of perforators larger than 1.5 mm (p < 0.01) and a 1.2-fold increase in the average diameter of the five largest perforators.
Body weight gain results in irreversible dilatation of the cutaneous perforators of the abdominal wall, with subsequent body weight loss not decreasing the size of perforators, facilitating optimal flap harvest in perforator flap surgery. Patients can therefore be advised to lose weight preoperatively, with benefit to both flap harvest and operative outcomes.
Parkville, Victoria, Australia
From the Jack Brockhoff Reconstructive Plastic Surgery Research Unit, Department of Anatomy and Cell Biology, the Department of Surgery, Royal Melbourne Hospital and University of Melbourne, and the Ludwig Institute for Cancer Research, Royal Melbourne Hospital.
Received for publication January 21, 2008; accepted May 29, 2008.
The first two authors contributed equally to this work.
Disclosure: The authors declare that there is no source of financial or other support or any financial or professional relationships that may pose a competing interest. The two first authors (R.S. and W.M.R.) are current Ph.D. candidates at the University of Melbourne and scholarship recipients of the Royal Australasian College of Surgeons.
Ramin Shayan, M.B.B.S., P.G.Dip.Surg.Anat., Angiogenesis Laboratory, Ludwig Institute for Cancer Research, Royal Melbourne Hospital Gratten Street, Parkville, Victoria, 3052 Australia, email@example.com