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Deldar et al. Plast Aesthet Res 2022;9:13 https://dx.doi.org/10.20517/2347-9264.2021.100 Page 3 of 16

debate among microsurgeons and is not routinely performed in many centers. Underlying
hypercoagulability can lead to microvascular thrombosis and subsequent flap failure with high rates of
nonsalvageability [21-23] . In 2015, our institution implemented a risk-stratified algorithm for perioperative
anticoagulation, whereby administration of heparin (subcutaneous or intravenous) following FTT is
determined by the presence of thrombophilic risk factors for microvascular thrombosis . Prior to
[22]
undergoing FTT, high-risk patients undergo a hypercoagulable workup, including a thrombophilia panel
and thorough history taking, to assess for any personal or family history of thromboembolism. Table 1
outlines the components of a thorough thrombophilia screening panel. Our group previously reported that
61% of patients undergoing FTT to LE reconstruction had at least one hypercoagulable trait; the most
common traits were plasminogen activator inhibitor-1 4G/5G variant and methylenetetrahydrofolate
[23]
reductase (MTHFR) A1298C and C677T polymorphisms . In addition, in patients with documented
thrombophilia, the use of a weight-based heparin drip titrated to a goal partial thromboplastin (PTT) of 50-
[22]
70 s decreased flap failure from 19% to 3% .

Wound bed preparation
From a surgical perspective, aggressive debridement and wound bed preparation is the first step in wound
management. Serial excisional debridements are required until all infected or devitalized tissue and biofilm
have been removed [24,25] [Figure 1]. Wide excision to a healthy wound bed is necessary, as there is up to a
six-fold increase in amputation if the wound is closed with positive post-debridement cultures among
[26]
diabetic patients undergoing LE FTT . Poor host defenses, high glucose levels, and periwound blood
supply likely amplify the effect of residual bacterial colonization on the ultimate reconstructive outcome .
[27]
Aerobic and anaerobic cultures are obtained deep to the wound surface before and after each debridement.
Infectious disease (ID) specialists are consulted to assist in culture-driven antibiotic therapy. Antibiotics
should be continued until cultures are negative; at this time, a patient is deemed ready for soft tissue
reconstruction from an ID standpoint.

In addition, in our operating rooms, we use a two-table setup of sterile instruments in the operating room,
including glove exchange to reduce instrument cross-contamination during excisional debridement and
coverage or closure of infected wounds . Using a two-table setup, we found a 78% absolute risk reduction
[28]
[28]
in cross-contamination . Therefore, it is critical to avoid recontamination of a surgically debrided wound
as reinfection could lead to devastating sequelae.

Biomechanical principles
Prior to wound closure, patients should undergo biomechanical examination and gait analysis with
podiatric and/or orthopedic surgery to identify mechanical factors that may contribute to wound
development or recurrence if not addressed. Any foot or ankle deformity, in conjunction with diabetic
neuropathy, can increase the risk of DFU development [29,30] . Peripheral neuropathy is characterized by loss
of protective sensation and proprioception, muscle weakness, and imbalance; all of these can contribute to
increased plantar pressures during gait [31-34] . Contracture of the Achilles tendon causes limited joint mobility
at the ankle, defined as equinus deformity. This has been implicated as a major factor in the development of
midfoot Charcot collapse and plantar ulcer formation [34-37] . We routinely address equinus gait with Achilles
tendon lengthening, which has been shown to reduce DFU recurrence by up to 95% in this population .
[38]
Biomechanical foot and ankle stabilization may require surgical intervention, including tendon transfers,
minor bony amputation, or Charcot realignment and stabilization. Calcaneal gait, characterized by
increased ankle dorsiflexion during midstance, is another manifestation of Charcot foot . Calcaneal ulcers
[39]
are difficult to heal and usually require surgery to correct the deformity causing the ulcer .
[40]