Discussion: Selective Intraoperative Vasopressor Use Is Not Associated with Increased Risk of DIEP Flap Complications

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Most microsurgeons prefer to avoid using intraoperative vasopressors because of a theoretical concern for vasospasm leading to vascular thrombosis and flap loss. However, systemic hypotension, which can occur in as many as 40 to 60 percent of patients undergoing general anesthesia, can lead to hypoperfusion of vital organs and free flaps.1 Conclusions from prior experimental and clinical series about the safety of vasopressors in microvascular free flap surgery have been contradictory.
Szabo Eltorai et al.2 examine the effect of vasopressors in 98 of a series of 333 consecutive patients undergoing deep inferior epigastric perforator (DIEP) flap breast reconstruction who received either ephedrine or phenylephrine. They concluded that vasopressors used in their experience do not cause anastomotic or pedicle thrombosis and do not appear to cause clinically significant flap tissue damage, such as fat necrosis, based on 60-day reoperation rates. In fact, they found an association between ephedrine and lower intraoperative rates of vasospasm, thrombosis, and venous congestion requiring revision (OR, 0.88), probably because of its selective beta-1 agonist effects. Selective beta-1 agonist activity results in improved cardiac output with less systemic vasoconstriction compared with phenylephrine, which is a direct alpha-1 agonist. A limitation is that the authors were not able to retrospectively identify the exact timing of vasopressor administration with respect to whether it was given before, during, or well after the vascular anastomosis.
Our own unpublished experience includes vasoactive substance use (including ephedrine, phenylephrine, and calcium chloride) in 4816 of 5671 consecutive breast, head and neck, and extremity free flap cases and, similarly, demonstrates that vasoactive substances had no effect on pedicle compromise (adjusted OR, 0.73; 95 percent CI, 0.5 to 1.07; p = 0.106) or flap failure (adjusted OR, 0.69; 95 percent CI, 0.41 to 1.16; p = 0.173).3 Rather, there was significantly less risk of venous congestion (adjusted OR, 0.60; 95 percent CI, 0.39 to 0.92; p = 0.018) associated with use of a vasoactive substance. There was no significant association between pedicle compromise or flap loss and vasoactive substance use even when broken down to the periods between induction up to 30 minutes before the anastomosis, 30 minutes before up to 30 minutes after the anastomosis, and 30 minutes after the anastomosis to the end of surgery.
The authors should be congratulated for putting a clinically important controversy to rest. Our own prior investigations suggest that vasospasm is rarely, if ever, an isolated cause of free flap compromise or failure, with technical problems associated with pedicle tension, kinking, or twisting; intraoperative pedicle or perforator injury; and postoperative events such as thrombosis secondary to infection or pedicle compression being the most common causes.4–6 As Szabo Eltorai et al. point out, widespread use of topical vasodilators, such as papaverine, and the short duration of action of vasoactive substances, make it unlikely that vasospasm is a major factor in free flap compromise and loss.
A caveat is that the present study, and our own experience, do not answer at what dosage or frequency ephedrine or phenylephrine administration results in irreversible tissue damage to the flap and whether free flaps are indeed more sensitive to vasopressors than other organs or tissues because they have no collateral vascularization.
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