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Page 10 of 15 Inchauste. Plast Aesthet Res 2023;10:27 https://dx.doi.org/10.20517/2347-9264.2022.139

demonstrated free flap survival and thrombotic complication did not improve with routine use of dextran
40 and had an increased risk of other systemic complications [50,52,53] . Dextran 40 is no longer routinely used
during standard autologous free flap breast reconstruction. However, for patients with a known
[52]
hypercoagulable state, Dextran 40 has been described for thrombosis prevention .

Antiplatelet medication:

Antiplatelet therapy such as aspirin has been used as prophylaxis against thrombus in microvascular free
flap surgery. Aspirin or acetylsalicylic acid inhibits cyclooxygenase, decreasing the production of
arachidonic acid metabolism, including TxA2, a potent platelet aggregator and vasoconstrictor, thus
inhibiting thrombus formation. Aspirin has been effective in the prevention of thrombus formation
[16]
associated with cerebrovascular events and myocardial infarction . Most recent studies demonstrated no
significant reduction of thrombosis or flap failure with the use of aspirin but did increase the risk of
hematoma [54,55] . These more recent studies have shifted the routine use of antiplatelet therapy to more
restricted use for high-risk patients.

Patients with a history of unprovoked thromboembolic events, multiple miscarriages, or a known
hypercoagulable state can successfully undergo autologous free flap breast reconstruction. However, the
patients should be counseled on the risk of flap failure, reoperation, prolonged hospitalization, need for
systemic anticoagulation, use of antiplatelet therapy, increased risk of bleeding complications, and
[56]
significant risks of other thromboembolic events such as DVT, PE or stroke . Consideration of hematology
consultation and coagulopathy work-up before surgery can aid in the formulation of a proper
anticoagulation plan to maximize success in this patient population. Hypercoagulability is a relative
contraindication for autologous free flap breast reconstruction but not an absolute contraindication.

MANAGEMENT
Up to about 5%-6% of autologous breast free flap reconstructions require operative exploration for vascular
compromise [26,57] . Venous thrombosis is the most common cause of flap compromise, followed by arterial
compromise, then hematoma or infection [48,57] . Timely recognition of vascular compromise is critical to flap
survival, and early intervention is associated with higher flap salvage rates [16,57-59] . Intraoperative recognition
and revision have significantly better prognoses and lower flap loss rates . However, flap salvage rate has
[48]
been shown to be highest within the first 24 h of the initial surgery with close to 94% salvage rates and
[26]
drops considerably further during the postoperative period, down to 12.1% salvage rate by postoperative day
3 [12,26] . Improved salvage rates are associated with early intervention, the use of alternative recipient vessels,
and fewer microsurgical revisions . Close flap monitoring is most crucial in the first 24 h postoperatively
[60]
to detect flap compromise [Figure 4], and if vascular thrombosis is suspected, then immediate return to the
operating room is indicated.

Troubleshooting a failing free flap starts with distinguishing between arterial and venous compromise. The
next step is to identify the cause of the problem and the mechanisms to correct the problem. The
anastomosis can have technical issues such as intimal injury, a back walled suture in the anastomosis or
inadequate recipient vessel. Mechanical problems such as hematoma, seroma, tight inset, pedicle kink or
twist can all impair vascular flow. Problems within the flap include damaged perforators or pedicle,
superficial dominant venous system with engorged SIEV and venous congestion with dark dermal bleeding.