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Delay Procedure in the perforasome era: A case in a DIEAp Flap


Authors: P. Hyza 1;  Lombardo G. A. G. 2;  T. Kubek 1;  Z. Jelínková 1;  J. Veselý 1;  R. Perrotta 2
Authors‘ workplace: Department of Plastic and Reconstructive Surgery, St Anne’s University Hospital, Brno, Czech Republic 1;  Department of Plastic and Reconstructive Surgery, University of Catania, Cannizzaro Hospital Catania, Italy 2
Published in: ACTA CHIRURGIAE PLASTICAE, 57, 1-2, 2015, pp. 24-26

INTRODUCTION

The deep inferior epigastric artery perforator (DIEAp) flap has become an increasingly popular choice since its introduction in 19891 and it is one of the most commonly used perforator flaps for breast reconstruction.

Despite the huge use of the DIEAp flap in the reconstructive field, an evidence based approach in perforator selection has not yet been developed2. Unfortunately there is no clear evidence about the relation between the number and dimension of the perforator vessel and the prediction of flap survival.

Vascular delay, also known as the delay phenomenon, is the rendering of a tissue ischemic to increase vascularity before transfer. This improves flap survival, increases the length-to-breadth ratio in random pattern flaps, and allows for the reliable transfer of greater volumes of tissue in axial pattern flaps8.

It is unusual to talk about delay in the perforasome era but this procedure could be extremely useful in the cases where the vascularity of the perforasome is precarious6.

In this paper we report the use of a delay procedure after the dissection of a DIEAp flap and we show the perforasome changes in the early time.

CASE REPORT

A 40-years-old woman underwent delayed breast reconstruction with a DIEAp flap. The flap was based on three perforators of the lateral row (1.5–2 mm). During the dissection of a DIEAp flap the choice of the perforator is a crucial step and we prefer, when it is possible and when there is not a dominant perforator (≥ 4 mm), to include more than one perforator in the same row, and thereby increasing the blood supply to the flap.

After the elevation, the flap appeared poorly perfused right away, especially in the zone II-IV3 (Fig. 1). In the zone I–III the flap appeared jeopardized especially in the caudal part and only the cranial zone was well perfused.

Fig. 1. The post-operative aspect of the flap. After the elevation, the flap appeared right away not well perfused especially in the zone II-IV. In the zone I-III the flap appeared jeopardized especially in the caudal part and only the cranial zone was well perfused
Fig. 1. The post-operative aspect of the flap. After the elevation, the flap appeared right away not well perfused especially in the zone II-IV. In the zone I-III the flap appeared jeopardized especially in the caudal part and only the cranial zone was well perfused

We decided to wait 45 minutes to see if there were any changes in the appearance of the flap. Unfortunately no change occurred and we decided to resort to the delay procedure. The flap was maintained in situ and we performed a primary tension-free suture of the fascia with a running non-absorbable 1/0 suture, as well as a skin suture of the flap and of the breast pocket prepared at the same time with the recipient vessels (IMA/IMV).

After 96 hours the perfusion of the flap improved (Fig. 2). An enlargement of the perforasome occurred, overcoming the midline. We decided to transfer the flap after 4 days when the dimension of the surviving flap was enough to restore the mastectomized breast.

Fig. 2. The aspect of the flap after 96 hours. An enlargement of the perforasome occured, overcoming the midline
Fig. 2. The aspect of the flap after 96 hours. An enlargement of the perforasome occured, overcoming the midline

The inset of the flap was more difficult than usually due to edema and stiffness. No infection, hematoma, or partial or complete flap necrosis were observed after the procedure. The patient was discharged home on the ninth post-operative day.

DISCUSSION

The studies on perfusion territory show a discrepancy in findings between vascular mapping studies and clinical observation because they do not take into account the physiological changes in the vasculature that occur in a living patient4–5; The perforasome theory explains how the skin areas are linked among them by direct vessels and indirect vessels (recurrent flow from subdermal plexus)6.

Unfortunately there is no clear evidence about the relation between the number and dimension of the perforator vessel and the prediction of flap survival.

In cadaveric studies on comparison of the perfusion of the commonly used abdominal flap in breast reconstruction4–5, the lateral row perforator DIEAp flaps crossed the midline only in certain cases, underestimating the consistent perfusion across the midline seen in vivo. Actual vascularity may be quite different in a physiological situation, where nervous, hormonal, and local controls of the vessels come into play.

Our case is demonstrating these changes and an enlargement of the perforasome that crosses the midline that occurred in the flap.

Delay procedures, previously used especially for pedicled TRAM flap3,7, have not been widely studied in free flaps, probably because of the inherent complexity and the robust vascularity of free tissue transfer 8 although previously a “delay modified” procedure in DIEAp flap was used, maintaining a skin bridge to increase the vascular supply from subdermal plexus (indirect vessels)10.

Usually the delay lasts one week or more 9 but in the first few days (24–72h) the early effect of the delay occurs with a reduction of the hyperadrenergic state post-elevation and a dilation of the choke vessels connecting the skin areas8–9.

Our flap was based on three perforators from the lateral branch of the DIEA. Usually the lateral row ensures a good perfusion, especially in zone I and III. Surprisingly in this case the perfusion was poor also in the zone I and III.

Although we waited about 45 minutes after the dissection of the flap to solve the deficiency in blood supply, probably due to a vasospasm, the perfusion did not improve. For this reason we think that the shortfall in blood supply was more likely due to a small perforasome, rather then to a vasospasm.

We believed that transferring the flap directly, despite a precarious vascularization, was risky.

Therefore we chose to delay the transfer waiting for an enlargement of the perforasome in situ, exploiting especially the early effects of the delay phenomenon.

The most of partial flap loss and fat necrosis in DIEAp flap could be caused by a lack of knowledge about the perforasome after the dissection and how it changes during the time, especially in the first 24–72 hours.

Although the DIEAp perfusion territory on cadaver has already been studied, further speculations are necessary to investigate the changes of the perforasome in vivo.

CONCLUSION

In conclusion we believe that vascular delay should be part of the armamentarium of any reconstructive microsurgeon; it could be used as lifeboat procedure when the vascular supply is inadequate and the surgeons do not feel confident about the flap’s perforasome.

Corresponding Author:

Giuseppe A.G. Lombardo M.D.

Department of plastic surgery, University of Catania

Cannizzaro Hospital

Via messina 829, Catania 95100

E-mail: giuseppelombardouni@gmail.com


Sources

1. Koshima I, Soeda S. Inferior epigastric artery skin flaps without rectus abdominis muscle. Br J Plast Surg. 1989;42:645–8.

2. Ireton JE1, Lakhiani C, Saint-Cyr M. Vascular anatomy of the deep inferior epigastric artery perforator flap: a systematic review. Plast Reconstr Surg. 2014 Nov;134(5):810e-21e.

3. Hartrampf CR, Scheflan M, Black PW. Breast reconstruction with transverse abdominal island flap Plast Reconstr Surg. 1982;69:216–25.

4. Wong C, Saint-Cyr M, Arbique G, et al Three- and four- dimensional computed tomography angiographic studies of commonly used abdominal flaps in breast reconstruction. Plast Reconstr Surg. 2009;124:18–27.

5. Wong C, Saint-Cyr M, Mojallal A, Schaub T, M.D. Bailey SH, Myers S, Brown S, Rohrich RJ. Perforasomes of the DIEP Flap: Vascular Anatomy of the Lateral versus Medial Row Perforators and Clinical Implications. Plast Reconstr Surg. 2010;125:772.

6. Saint-Cyr M, Wong C, Schaverien M, Mojallal A, Rohrich RJ. The perforasome theory: Vascular anatomy and clinical implications. Plast Reconstr Surg. 2009;124:1529–44.

7. Millard DR Jr. Breast reconstruction after a radical mastectomy Plast Reconstr Surg. 1976;58:283–91.

8. Ghali S, Butler PEM, Tepper OM, Gurtner GC. Vascular Delay. Plast Reconstr. Surg. 2007;119:1735.

10. Christiano JG, Rosson GD. Clinical experience with the delay phenomenon in autologous breast reconstruction with the deep inferior epigastric artery perforator flap Microsurgery. 2010 Oct;30(7):526–31.

Labels
Plastic surgery Orthopaedics Burns medicine Traumatology
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