- Email: [email protected]
Free flap survival after traumatic pedicle avulsion in an obese diabetic patient
Correspondence and communications 3. Mathes SJ, Steinwald PM, Foster RD, et al. Complex abdominal wall reconstruction: a comparison of flap and mesh closure. Ann Surg 2000;232:586e96. 4. Bleichrodt RP, Simmermacher RK, van der Lei B, et al. Expanded polytetrafluoroethylene patch versus polypropylene mesh for the repair of contaminated defects of the abdominal wall. Surg Gynecol Obstet 1993;176:18e24. 5. Ramirez OM, Ruas E, Dellon AL. ‘‘Components separation’’ method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg 1990;86:519e26. 6. Maas SM, de Vries RS, van Goor H, et al. Endoscopically assisted ‘‘components separation technique’’ for the repair of complicated ventral hernias. J Am Coll Surg 2002;194:388e90. 7. Vargo D. Component separation in the management of the difficult abdominal wall. Am J Surg 2004;188:633e7. 8. Sukkar SM, Dumanian GA, Szczerba SM, et al. Challenging abdominal wall defects. Am J Surg 2001;181:115e21. 9. Ewart CJ, Lankford AB, Gamboa MG. Successful closure of abdominal wall hernias using the components separation technique. Ann Plast Surg 2003;50:269e73 [discussion 73e4]. 10. de Vries Reilingh TS, van Goor H, Rosman C, et al. ‘‘Components separation technique’’ for the repair of large abdominal wall hernias. J Am Coll Surg 2003;196:32e7. 11. Ramirez OM. Inception and evolution of the components separation technique: personal recollections. Clin Plast Surg 2006; 33:241e6. vi. 12. Thomas III WO, Parry SW, Rodning CB. Ventral/incisional abdominal herniorrhaphy by fascial partition/release. Plast Reconstr Surg 1993;91:1080e6. 13. Voigt M, Andree C, Galla TJ, et al. Reconstruction of abdominal-wall midline defects e the abdominal-wall components separation. Zentralbl Chir 2001;126:1000e4. 14. Reid RR, Dumanian GA. Panniculectomy and the separation-ofparts hernia repair: a solution for the large infraumbilical hernia in the obese patient. Plast Reconstr Surg 2005;116: 1006e12. 15. Dumanian GA, Denham W. Comparison of repair techniques for major incisional hernias. Am J Surg 2003;185:61e5. 16. Girotto JA, Ko MJ, Redett R, et al. Closure of chronic abdominal wall defects: a long-term evaluation of the components separation method. Ann Plast Surg 1999;42:385e94 [discussion: 94e95].
999 17. Howdieshell TR, Proctor CD, Sternberg E, et al. Temporary abdominal closure followed by definitive abdominal wall reconstruction of the open abdomen. Am J Surg 2004;188:301e6. 18. Schecter WP, Ivatury RR, Rotondo MF, et al. Open abdomen after trauma and abdominal sepsis: a strategy for management. J Am Coll Surg 2006;203:390e6. 19. van Geffen HJ, Simmermacher RK, van Vroonhoven TJ, et al. Surgical treatment of large contaminated abdominal wall defects. J Am Coll Surg 2005;201:206e12.
Tarek Abulezz Department of Plastic Surgery, Faculty of Medicine, Sohag University, Sohag 82524, Egypt E-mail address: [email protected] ª 2008 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.12.033
Free flap survival after traumatic pedicle avulsion in an obese diabetic patient A 48-year-old female sustained a full thickness burn to her right heel from prolonged contact with a motorbike exhaust. The patient was a diabetic non-smoker. The burn, involving bone, was debrided and a Vacuum Assisted Closure (VAC) dressing applied. Coverage was achieved using a (six by five cm) free radial forearm flap, chosen as the defect required a thin flap. The radial artery was anastomosed end-to-end to the posterior tibial artery and two venous anastomoses were performed to the venae comitantes. The postoperative course was uneventful. At 26 days the patient sustained an open calcaneal fracture (Figure 1a) from a dorsiflexion injury, with the flap
Figure 1 a) Lateral radiograph demonstrating calcaneal fracture. b) The radial forearm flap following trauma with its avulsed pedicle and proximal skin attachments.
1000
Correspondence and communications
Figure 2
The result at four months.
being completely avulsed at its pedicle and its proximal soft tissue attachments (Figure 1b). The flap rapidly became congested. The fracture was fixed using percutaneous cannulated screws and the pedicle explored. The venous anastomoses were completely avulsed and the vessels were thrombosed. It was not possible to find the flap artery as avulsion had occurred within the substance of the flap. The flap was resutured without tension but remained brisk and dusky. A decision was made to treat the flap expectantly, and it was leeched for three days. 15 days later a small well demarcated proximal skin edge was debrided, a VAC dressing applied, and the defect was subsequently skin grafted. On review at four months the wound was almost fully healed (Figure 2). Salgado et al.1 reported a low free flap survival rate following late loss of arterial inflow (after perioperative day seven) if the recipient bed was compromised, due to impaired revascularisation from the flap periphery and bed. Of ten cases with a mean loss of arterial inflow of 52 days (due to anastomotic rupture (five cases), arterial occlusion (four cases) or avulsion (one case only)) five flaps survived, four were completely lost and one showed partial necrosis. Three of those that survived were on healthy recipient beds. All of the flaps that were partially or completely lost were on compromised beds. The authors suggested that free flap survival is reduced if there is poor condition of the recipient site due to trauma, ischaemia or scarring. Interestingly the flap where the pedicle was traumatically avulsed during surgery (at 100 days) mostly survived (66%) despite being inset onto a scarred bed, but the patient had no major comorbidity. The authors had decided not to revascularise the tissue after observation of a viable flap. The authors also found that the timing of late loss of arterial inflow was not the main determinant of flap survival. They recommended aggressive salvage attempts if the quality of the bed was poor as they felt that revascularisation was unlikely. In a large series of free flaps Wei et al.2 treated 63% of their failed extremity flaps conservatively, and found that this was a successful alternative to second free flaps
for partial and total losses, with most wounds healing. Weinzweig et al.3 suggested that free tissue failure is not an all-or-none phenomenon and that in their experience failing free flaps may be managed expectantly. In vivo porcine studies confirm that free flaps may survive (from the eight postoperative day) following ligation of their pedicle due to revascularisation from their recipient bed.4 However, these experimental flaps did not have compromised beds. We would not have anticipated free flap survival in our patient due to the presence of potential adverse factors, namely trauma, diabetes and obesity. With regards to the flap being revascularised prior to the avulsion of its pedicle, diabetes must not have compromised this process sufficiently to cause it to fail. Salgado et al.1 found that no major comorbidities correlated with late arterial inflow loss. In particular four of their ten patients who had loss of arterial inflow had diabetes. Two of these flaps survived and two were lost. These numbers are small and it is not possible to draw conclusions on the adverse contribution of diabetes to revascularisation. Although trauma appears to correlate with poor revascularisation and therefore flap non survival post interruption of arterial outflow,1 it may not cause flap death if the bed has already been revascularised. Factors present at the outset contributing to a poor quality bed, such as trauma or scarring, may be important. On the basis of this experience we would recommend initial conservative management of a late traumatically avulsed extremity free flap, with close monitoring, if the recipient bed was initially of a reasonable quality, despite the presence of adverse factors such as diabetes or obesity.
References 1. Salgado CJ, Smith A, Kim S, et al. Effects of late loss of arterial inflow on free flap survival. J Reconstr Microsurg 2002;18:579e84. 2. Wei FC, Demirkan F, Chen HC, et al. The outcome of failed free flaps in head and neck and extremity reconstruction: what is next in the reconstructive ladder? Plast Reconstr Surg 2001; 108:1154e60. 3. Weinzweig N, Gonzalez M. Free tissue failure is not an all-ornone phenomenon. Plast Reconstr Surg 1995;96:648e60. 4. Black MJ, Chait L, O’Brien BM, et al. How soon may the axial vessels of a surviving free flap be safely ligated: a study in pigs. Br J Plast Surg 1978;31:295e9.
Olivier Alexandre Branford Marcus Davis Frederik Schreuder Department of Plastic Surgery, Lister Hospital, Coreys Mill Lane, Stevenage, Hertfordshire SG1 4AB, UK E-mail address: [email protected] ª 2008 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2008.04.002
999 17. Howdieshell TR, Proctor CD, Sternberg E, et al. Temporary abdominal closure followed by definitive abdominal wall reconstruction of the open abdomen. Am J Surg 2004;188:301e6. 18. Schecter WP, Ivatury RR, Rotondo MF, et al. Open abdomen after trauma and abdominal sepsis: a strategy for management. J Am Coll Surg 2006;203:390e6. 19. van Geffen HJ, Simmermacher RK, van Vroonhoven TJ, et al. Surgical treatment of large contaminated abdominal wall defects. J Am Coll Surg 2005;201:206e12.
Tarek Abulezz Department of Plastic Surgery, Faculty of Medicine, Sohag University, Sohag 82524, Egypt E-mail address: [email protected] ª 2008 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2007.12.033
Free flap survival after traumatic pedicle avulsion in an obese diabetic patient A 48-year-old female sustained a full thickness burn to her right heel from prolonged contact with a motorbike exhaust. The patient was a diabetic non-smoker. The burn, involving bone, was debrided and a Vacuum Assisted Closure (VAC) dressing applied. Coverage was achieved using a (six by five cm) free radial forearm flap, chosen as the defect required a thin flap. The radial artery was anastomosed end-to-end to the posterior tibial artery and two venous anastomoses were performed to the venae comitantes. The postoperative course was uneventful. At 26 days the patient sustained an open calcaneal fracture (Figure 1a) from a dorsiflexion injury, with the flap
Figure 1 a) Lateral radiograph demonstrating calcaneal fracture. b) The radial forearm flap following trauma with its avulsed pedicle and proximal skin attachments.
1000
Correspondence and communications
Figure 2
The result at four months.
being completely avulsed at its pedicle and its proximal soft tissue attachments (Figure 1b). The flap rapidly became congested. The fracture was fixed using percutaneous cannulated screws and the pedicle explored. The venous anastomoses were completely avulsed and the vessels were thrombosed. It was not possible to find the flap artery as avulsion had occurred within the substance of the flap. The flap was resutured without tension but remained brisk and dusky. A decision was made to treat the flap expectantly, and it was leeched for three days. 15 days later a small well demarcated proximal skin edge was debrided, a VAC dressing applied, and the defect was subsequently skin grafted. On review at four months the wound was almost fully healed (Figure 2). Salgado et al.1 reported a low free flap survival rate following late loss of arterial inflow (after perioperative day seven) if the recipient bed was compromised, due to impaired revascularisation from the flap periphery and bed. Of ten cases with a mean loss of arterial inflow of 52 days (due to anastomotic rupture (five cases), arterial occlusion (four cases) or avulsion (one case only)) five flaps survived, four were completely lost and one showed partial necrosis. Three of those that survived were on healthy recipient beds. All of the flaps that were partially or completely lost were on compromised beds. The authors suggested that free flap survival is reduced if there is poor condition of the recipient site due to trauma, ischaemia or scarring. Interestingly the flap where the pedicle was traumatically avulsed during surgery (at 100 days) mostly survived (66%) despite being inset onto a scarred bed, but the patient had no major comorbidity. The authors had decided not to revascularise the tissue after observation of a viable flap. The authors also found that the timing of late loss of arterial inflow was not the main determinant of flap survival. They recommended aggressive salvage attempts if the quality of the bed was poor as they felt that revascularisation was unlikely. In a large series of free flaps Wei et al.2 treated 63% of their failed extremity flaps conservatively, and found that this was a successful alternative to second free flaps
for partial and total losses, with most wounds healing. Weinzweig et al.3 suggested that free tissue failure is not an all-or-none phenomenon and that in their experience failing free flaps may be managed expectantly. In vivo porcine studies confirm that free flaps may survive (from the eight postoperative day) following ligation of their pedicle due to revascularisation from their recipient bed.4 However, these experimental flaps did not have compromised beds. We would not have anticipated free flap survival in our patient due to the presence of potential adverse factors, namely trauma, diabetes and obesity. With regards to the flap being revascularised prior to the avulsion of its pedicle, diabetes must not have compromised this process sufficiently to cause it to fail. Salgado et al.1 found that no major comorbidities correlated with late arterial inflow loss. In particular four of their ten patients who had loss of arterial inflow had diabetes. Two of these flaps survived and two were lost. These numbers are small and it is not possible to draw conclusions on the adverse contribution of diabetes to revascularisation. Although trauma appears to correlate with poor revascularisation and therefore flap non survival post interruption of arterial outflow,1 it may not cause flap death if the bed has already been revascularised. Factors present at the outset contributing to a poor quality bed, such as trauma or scarring, may be important. On the basis of this experience we would recommend initial conservative management of a late traumatically avulsed extremity free flap, with close monitoring, if the recipient bed was initially of a reasonable quality, despite the presence of adverse factors such as diabetes or obesity.
References 1. Salgado CJ, Smith A, Kim S, et al. Effects of late loss of arterial inflow on free flap survival. J Reconstr Microsurg 2002;18:579e84. 2. Wei FC, Demirkan F, Chen HC, et al. The outcome of failed free flaps in head and neck and extremity reconstruction: what is next in the reconstructive ladder? Plast Reconstr Surg 2001; 108:1154e60. 3. Weinzweig N, Gonzalez M. Free tissue failure is not an all-ornone phenomenon. Plast Reconstr Surg 1995;96:648e60. 4. Black MJ, Chait L, O’Brien BM, et al. How soon may the axial vessels of a surviving free flap be safely ligated: a study in pigs. Br J Plast Surg 1978;31:295e9.
Olivier Alexandre Branford Marcus Davis Frederik Schreuder Department of Plastic Surgery, Lister Hospital, Coreys Mill Lane, Stevenage, Hertfordshire SG1 4AB, UK E-mail address: [email protected] ª 2008 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.bjps.2008.04.002