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N. Patel et al.
daunting prospect for the patient, and even minor
complications can be very challenging for patients
and family. Appropriate patient and staff education
in the preoperative period not only is key in preventing complications from arising, but also
increases the success of interventions that may be
required. In effect, the preoperative management
plan serves to set one up for the best possible success in managing any intraoperative or postoperative challenges that may arise.
It is helpful to think about complications in three
broad categories: (a) patient related, (b) donor site
related, and (c) free ap related. The best and most
effective management of complications is to prevent them from happening, and this is the central
aim of the preoperative workup. Patient-related
characteristics can contribute signicantly to anesthetic and surgical risk, as well as predispose the
patient to the development of complications in the
immediate postoperative period. These are well
characterized, and workup for these conditions is
described in other chapters of this book covering
medical and surgical assessment and optimization
as well as patient education. With respect to donor
site-related challenges, the choice of the reconstructive ap determines the donor site. It is prudent to
consider several donor sites in the same patient in
case of ap failure, or the need for alternative or
additional free tissue transfer. The chapter in this
book on surgical assessment describes an approach
to addressing possible risks. Finally, in regard to
free ap-related issues, Corbitt etal. [3] describe the
causes of head and neck free ap failure in their
series as follows: infection—25%, kinked or compressed pedicle—23%, ap design- and harvestrelated issues—15%, hemorrhage—7%, and
hypercoagulable disorders—5%. It is important that
the patient who is predisposed to infection or might
have an undiagnosed systemic clotting or bleeding
disorder is identied in the preoperative period. The
patient who has had previous free ap failures
should, in our opinion, be considered for a nutrition
screen and hypercoagulability workup prior to surgery. CT angiograms of the planned ap site as well
as the neck vessels may be of some benet in this
cohort of patients.
Management of ap complications will often
involve a return to the operating room with the
need for salvage procedures and, in the event of
catastrophic failure, institution of the “reverse
reconstructive ladder” [4]. The surgeon should
understand that the likely alternative treatments
could involve, in descending order of preference,
a second free ap, a regional ap, conservative
care with debridement and closure with local
aps, and skin grafts or healing via secondary
intention. In some cases, a combination of several of these modalities may be required [5].
Intraoperative Phase
Intraoperative complications for free tissue transfer have been well established in the literature, and
common intraoperative causes of ap failure must
be noted by the treating surgeon so that steps can
be taken to avoid them or at the very least minimize them. Several factors must be considered,
and these include prolonged operative time, morphology and position of the vascular pedicle at the
recipient site, patients who have been previously
irradiated in the recipient site, the surgeon’s level
of experience, operative techniques, the incidence
of vessel spasms, formation of thromboses, as well
as the development of hematomas.
Prolonged Operative Time
A prolonged operative time has been identied as
an independent risk factor for failure in head and
neck free ap surgery. In a retrospective national
database study conducted by Ishimaru et al. [6],
2846 patients were identied and found that a prolonged operative time was signicantly associated
with free ap failure. Serletti etal. [7] reported that
an operative time longer than 10h was associated
with an increased risk of postoperative complications including thrombosis, hematoma, bleeding,
and ultimately free ap failure. Longer operative
times resulting in prolonged ischemic periods
increase the incidence of ap damage due to tissue
hypoxia and anoxia [8]. In order to reduce operative
and ischemic times, a two-team approach and the
availability of dual-recipient vessels, especially in
irradiated patients, are recommended.
Surgeon’s Expertise
It has been reported that surgical technique constitutes the most important component of free
6 Free Flap Considerations andComplications
97
ap success [9]. In a study by Zhou etal. [10],
the two surgeons who performed the microvascular anastomoses (XP and YW) both had more
than 5 years of experience in microvascular
anastomosis, and thus had a standardized protocol: (1) selection of a recipient vessel of the
same diameter as the donor vessel, (2) removal
of the attached soft tissue from the anastomosis
site, (3) widening of the diameters of both the
donor and recipient vessels by pressing microforceps against the inner membrane of the vessels, (4) irrigation with heparin before
anastomosis, (5) gentle suturing of the vessels
without tension, (6) checking the patency after
vessel anastomosis, (7) adjusting the position of
vessels to ensure no blind bend, and (8) use of
papaverine to prevent vasospasm. Good vessel
selection plays a signicant role in the success
of free tissue transfer. Most surgeons agree that
the facial and superior thyroid arteries, as well
as the common facial vein and internal jugular
vein branches, are the most suitable for anastomosis. In a study conducted in Shanghai covering a 34-year period and including 4640 aps,
authors showed that the facial and superior thyroid vessels were the most reliable, as these vessels are in close proximity to head and neck
defects and the caliber of these vessels is similar
to that of the donor vessels often used in reconstruction [11]. Having said this, irradiated
patients can demonstrate signicant changes in
vessel quality, with increased friability, intimal
changes, and calcications, and as such, these
vessels may not be adequate for anastomosis. In
this case, the surgeon must be prepared to
change vessels, electing to use the external
carotid artery, contralateral vessels, ipsilateral
transverse cervical vessels, or internal mammary vessels for anastomosis. The ability to
pivot in this scenario becomes crucial to achieve
higher success rates. It is important to note that
the choice of ap type has not been associated
with changes in free ap success rates. Kwok
and Agarwal [12] examined overall ap failure
rates based on the ap type (muscle, fascial,
skin, bone, and bowel ap) in 1187 cases and
concluded that there were no signicant associations between ap type and known risk factors
for ap failure (p=0.464).
Vessel Spasm andThrombosis
There are several causes of vessel spasms and
thrombosis, in both arterial and venous systems, and these must be considered in all cases
of free tissue transfer. First, hypotension is
considered a common cause of arterial thrombosis in free ap transfers, with the reduction
in blood ow through the anastomosed vessel
increasing the propensity of thrombosis. A
thrombosed artery will often appear as a bulge
at the thrombosed site, many times permitting
visual identication of the thrombus. Moreover,
the use of a handheld Doppler will conrm
whether blood ow is present or not. A second
risk factor for thrombosis is called “back-walling,” where the opposite side of the arterial
wall is sutured by mistake, resulting in intimal
damage and potential thrombosis. Vessel
spasms in and of themselves also serve as risk
factors for the development of clots, as they
can stagnate blood ow. Another cause for
arterial thrombosis is the presence of bends or
inadequate removal of the attached tissue from
the donor and recipient vessels. Therefore, if
the handheld Doppler conrms inadequate
blood ow after anastomosis, the surgeon must
take steps to rectify the situation. This involves
communication with the anesthesia team to
increase the mean arterial pressure, applying
papaverine to the anastomosis site, removal of
excessive fascial tissue from the anastomosed
vessel, as well as checking for any kinking in
the vessels. If after all of this blood ow is still
inadequate, anastomosis should be opened and
redone, while checking for intimal damage and
cutting back or changing vessels when necessary. The application of papaverine during
anastomosis has been found to increase carotid
artery blood ow in humans [13]. Similarly, it
has been found that the local application of
papaverine during vascular anastomosis could
sustain anastomotic dilatation. In a systematic
review of 20 articles, Vargas et al. [14] concluded that papaverine could produce a 66%
increase in vessel diameter, and that it possesses signicant vasodilatory effects on nonspastic vessels [15]. Papaverine acts directly
on calcium channels causing a direct increase
in cyclic adenosine monophosphate and subse-
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N. Patel et al.
quent increases in secondary messengers that
leads to protein kinase activation and nonselective smooth muscle relaxation and vessel dilation. One practical way to reduce vessel spasm
is to inject papaverine or lidocaine into the fascia of the pedicle during ap harvest. It is also
important to mention that thrombosis will
occur if the vessel endothelium is not intact
during anastomosis; therefore, it is important
to protect the intima without interruption or
damage during anastomosis.
Venous failure can also occur due to compression, spasm, and thrombosis and is a common
cause of intraoperative ap complications, as
venous thrombosis occurs more frequently than
arterial thrombosis. It is often very easy to kink or
twist the vein during or after anastomosis, and
careful attention should be paid to prevent this.
Additionally, the choice of an adequate recipient
vein is very important for ap success, with good
vessel caliber matching and a tensionless anastomosis playing an important role. While the external jugular vein is often very easily accessible,
sometimes authors do not recommend its use due
to its supercial position in the neck with the risk
of being easily compressible. Despite this, in our
experience with the external jugular vein, we have
not found this to be the case and have represented
a reliable recipient vein. However, the lingual vein
should also be avoided, as anastomosis to this vein
may be difcult due to its cranial position under
the mandible. At the conclusion of surgery, special
attention should be made to monitor the patient
while the anesthesia team is extubating the patient.
As the patient emerges from anesthesia, it is
important to stabilize the neck and observe for
rises in the patient’s blood pressure, as well as prevent patients from moving about forcefully, as
these can result in increases in intravascular pressure, with the risk of bleeding and subsequent
hematoma formation, which could lead to venous
compression and thrombosis.
Intraoperative Fluid Administration
Another critical risk factor associated with intraoperative free ap failure is excessive intraoperative uid administration. Haughey et al. [16]
hypothesized that edema of the ap or recipient
site can result from increased volumes of crystalloids, reporting a critical cutoff value of 7l of
crystalloids during surgery, with volumes higher
than this linked to major ap complications.
Moreover, Ruttmann etal. [17] suggested that the
use of crystalloids, as compared to colloids, can
result in a hypercoagulable state, especially when
administered rapidly, thus increasing the risk of
thrombosis intraoperatively. In their study,
Brinkman et al. [18] recommended that basic
uid maintenance should not exceed 6 cc/kg/h
and that normovolemic hemodilution is preferred, reporting that blood with a reduced hematocrit has a better ow prole than blood with a
normal hematocrit.
Use ofVasopressors
The concept of vasopressors increasing the risk
of free ap compromise has been one that has
been discussed extensively for decades. Several
studies have shown that intraoperative use of
vasopressors does not increase the risk of free
ap compromise and failure in head and neck
cancer patients. In a retrospective study performed with 47 patients undergoing free tissue
transfer for head, neck, and extremity reconstruction, Kelly etal. [19] reported that free ap survival was 97%, with 53.2% of cases showing the
use of intraoperative vasopressors. There was no
signicant difference in the frequency of total or
partial ap necrosis between patients who
received intraoperative vasopressors and those
who did not. Similarly, there was no statistical
signicance in the rate of arterial or venous
thrombosis between the two groups (p = 0.095
and p = 0.095, respectively). In another study,
Gardner etal. [20] reported that the use of vasopressors for extensive periods intraoperatively
during free ap surgeries had no association with
the rate of reoperation within 5days of intervention, regardless of the type of vasopressor used,
simultaneous use of multiple agents, and/or type
of free ap surgery. This study included 449 free
ap reconstructions with a total of 174 patients
receiving continuous vasopressors during their
reconstruction.
6 Free Flap Considerations andComplications
99
Postoperative Phase
By and large, the immediate postoperative period
represents the most common time for complications to occur in free ap reconstruction. Close
monitoring of patients in this time frame is crucial, as problems that are recognized and
diagnosed early have much higher rates of successful salvage.
Vascular Thrombosis
Vascular thrombosis is a devastating complication in free ap surgery, with thrombosis rates in
the literature ranging from 3.2% to 9.9% across
various studies, with an average occurrence in
6.4% of free aps [21], and this represents a
major contributor to free ap failure [22, 23].
Thrombosis can occur either at the level of the
pedicle or distally up to and including the microcirculation of the ap, and they can occur within
the venous system, the arterial vessels, or a combination of the two. Salvage rates in these
instances vary anywhere from 28% to 90%,
depending on the etiology of the complication
and the timing of salvage procedure [24]. Salvage
in cases of venous thrombosis is signicantly
higher than in arterial thrombosis, partially attributed to the fact that compromised aps due to
venous congestion are more likely to occur within
the rst 72 h and are often easier to detect, as
compared to arterial insufciency, which is a
more common cause of ap failure after the rst
72 h [25, 26]. The rates of salvage when both
venous and arterial systems demonstrate thromboses are, as expected, much lower [27]. Selber
et al. [28] demonstrated that mean ap salvage
rates in patients with microvascular ap compromise were 73% when returning once to the operating room, 34% when returning twice, and 27%
when returning three times, declining with
greater number of insults to the ap. The greatest
chance of success will be in patients with a technical failure that is identied early, with an immediate return to the operating room. The time
effect on salvage rates is likely associated with
several factors, including irreversible ischemic
injury to the ap and reperfusion injury with the
“no-reow” phenomenon after vascular patency
has been re-established, and these are closely
linked to secondary ischemia of the ap [29].
Primary ischemia is dened as the time between
division of the vascular pedicle and reestablishment of blood ow after anastomosis.
While generally accepted that the upper limit of
this is approximately 4h, it is ideal that this time
is kept under 60min. This also varies on the type
of ap, as aps involving muscle are more metabolically demanding and often do not tolerate
more than 3h of ischemia time, while the rate of
fat necrosis in aps such as deep inferior epigastric artery (DIEP) aps increases after primary
ischemia time exceeds 2h [30]. The concept of
secondary ischemia is one which is characterized
by the time between the occurrence of vascular
thrombosis and return of blood ow to the ap,
most often after nonsurgical or surgical intervention. It has been described that secondary ischemia can be much more devastating for ap
survival than the primary ischemic period, secondary to increases in interstitial edema, platelet
and brinogen concentrations, and increased
rates of thrombosis [31, 32]. Furthermore, it has
also been shown that the time between primary
and secondary ischemia also inuences rates of
ap survival. If the period between ischemic episodes is less than 24h, secondary ischemia results
in signicantly more ap necrosis than if that
inter-ischemic period was stretched to 72 h or
more, likely linked to increased time to washout
of damaging free radicals from primary ischemia
[33]. Reperfusion injury is an inammatory process which occurs when restored blood ow after
a period of ischemia allows the inux of accumulated inammatory and damaging substrates such
as free radicals that can injure the ap and
severely compromise its survival. The transition
point between normal reperfusion and reperfusion injury is poorly dened and differs among
various tissue types, with some tissues being
more resistant to ischemia than others, as previously mentioned. For all tissues, however, the
longer the periods of ischemia, the more likely
they are to result in irreparable damage to the
microcirculation and to the ap tissues. Stotland
and Kerrigan [34] described damage caused by
reperfusion injury as cell death by “bombard-
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N. Patel et al.
ment.” Neutrophils become activated, inammatory mediators accumulate, and oxygen-based
free radicals and proteolytic enzymes are
released, inducing tissue damage. The “noreow” phenomenon is often the result of reperfusion injury and was rst described in 1967 as
the “lack of nutritive capillary perfusion despite
reperfusion of ischemic tissue” [35]. There have
been several theories put forth on the physiologic
nature of this phenomenon, involving things such
as intravascular hemoconcentration, which
changes the rheostatic properties of the blood,
swelling of endothelial cells, increases in interstitial pressure and edema, and capillary obstruction
by leukocytes [36].
The time to re-exploration has varied in the
literature, ranging from peaking in the rst 24h
[37, 38] up to 80% occurring within the rst
5 days postoperatively [39]. Despite this, the
incidence of late thrombosis after postoperative
day 5 has been well documented and accounts for
between 10% and 28% of all thromboses [40,
41]. Free aps are thought to undergo revascular-
ization by way of the surrounding tissues and
have an increased ability to survive without pedicle ow within several days after surgery, and it
has been shown to result in complete ap independence as early as 6–8days postoperatively in
experimental animal studies [42–45]. As such,
some postulate that late thrombosis has a
decreased incidence of ap loss even with conservative management [46–48]. However, most
authors believe that revascularization can take
signicantly longer and can remain dependent of
pedicle ow for several months to years [49–51].
The surgeon must differentiate between a true
late thrombosis and delayed recognition of early
thrombosis, as the latter has much lower salvage
rates and likely accounts for the majority of
“late” thrombosis diagnoses. Both early and late
thromboses have been shown to be predominantly of the venous system. The type of ap has
also been studied in regard to rates of collateral
revascularization, with reports of osseous aps
having longer dependence on pedicle ow as
compared to soft tissue aps [52]. A major cause
of late thrombosis is infection [53], with increases
in the rate of thrombosis by 50–75% even up to
1 month postoperatively in this cohort [54]. A
study by Sweeny et al. described a shift in the
timing of free ap failures, demonstrating in their
cohort that only 40% of failures occurred within
the rst 72 h, with the majority of late failures
being arterial insufciency in nature. They postulate that while early venous failures are due to its
low-pressure characteristics being more susceptible to external compression and pedicle geometry, and early arterial failures are due to technical
issues (often found with intraoperative arterial
thrombosis as well), the later failures involving
arterial thromboses are more often due to the
poor quality of vessels, due to either presence of
calcications (Fig.6.1), plaques, or other vessel
wall compromise, which may also contribute to
the lower rates of salvage of these aps [55].
Venous thrombosis is by and large the most
common vascular complication that is encountered in the postoperative period in free ap surgery, accounting for as much as 70% of
indications for re-exploration, and often occurs
within the rst 48h [56]. This is likely due to the
fact that venous structures are more easily compressible by surrounding edema, hematoma formation, and/or tight skin closure; have higher
rates of spasm; and can result in vascular stasis
more easily with pedicle kinking and even transient periods of hypotension [57, 58]. Arterial
thrombosis, however, is most often associated
with technical factors at the level of the anastomosis, such as inadvertent damage to the intima
during vessel manipulation, exposing the subendothelial connective tissues to circulating platelets and triggering the hemostatic cascade [59].
Other issues may include poor vessel apposition/
mismatch, back-walling of the suture, vascular
twisting, vasospasm, calcications, as well as
undue tension or compression at the anastomotic
site, which can all contribute to clot formation
[60]. This can result in multiple attempts at
reanastomosis, resulting in prolonged ischemia
times, reperfusion injury, and “no-reow” phenomenon [61].
The earliest sign of venous congestion of a
ap is the appearance of hyperemia, a slight darkening of ap color in some areas with appearance
of pinpoint ecchymoses, with a “goosebump”
6 Free Flap Considerations andComplications
Fig. 6.1 Calcied
vessels in patients
receiving free ap
reconstruction
Fig. 6.2 Slight
darkening of ap color
with pinpoint
ecchymoses (blue arrow)
in early venous
congestion
101
appearance (Fig. 6.2). Eventually, this leads to
increased ap turgor with the ap appearing
tense, more generalized changes in color from
red to blue to purple (Fig. 6.3), brisk capillary
rell of <2s, and increased warmth of the ap. A
scratch or pinprick test can be performed to further assess the ap, which would reveal a rapid
return of dark-appearing blood (Fig.6.4), indicating a lack of outow of venous circulation.
Arterial insufciency of free aps appears quite
differently clinically than venous congestion,
with a decrease or arrest in inow of blood supply. This leads to ap that appears pale in color, is
soft with decreased turgor, would feel cool to the
touch, and have a prolonged capillary rell of
>2–3s. A scratch or pinprick test would reveal a
very slow (or even absent) return of blood, indicating a lack of inux of sufcient blood supply
(Fig.6.5).
In the setting of venous compromise, one can
consider bedside neck exploration under mild
sedation if no clinical signs of ap congestion are
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Fig. 6.3 Progression of
venous congestion to
more generalized blue/
purple color change, and
increased ap turgor
N. Patel et al.
Fig. 6.4 Pinprick test
reveals rapid return of
dark-red blood (blue
arrows) in venous
congested ap
seen in the skin paddle, and all that is seen is a
loss of the implantable Doppler signal, if one was
used, as oftentimes this may simply be a coupler
malfunction. If clinical signs of venous congestion are present in the ap, immediate take-back
to the OR for exploration is warranted. Even in
the case where return to the OR is planned, one
can consider opening sutures bedside to see if
taking some of the pressure off the venous circulation by surrounding edema, accumulation of
interstitial uid, or tight closure can potentially
help relieve the external compression. The surgeon can also open the neck entirely bedside to
visually examine the pedicle to see if there is a
kink or twist that can be rectied bedside. If an
obvious clot is present within the venous system,
one can also consider opening the venous anastomosis to allow the ap to drain, thereby decreasing the potential for ap damage until the patient
can be brought back to the OR for formal explo-
ab
6 Free Flap Considerations andComplications
Fig. 6.5 Pale-appearing
skin paddle, with
decreased turgor, with
minimal return of blood
on scratch test (blue
arrow), indicative of
arterial insufciency
Fig. 6.6 (a) Takedown
of ap to carefully
examine and inspect to
determine the cause of
venous congestion. (b)
Identication of venous
thrombosis (blue arrow)
103
ration. The surgeon can gently pack the neck with
gauze, while the ap continues to drain until
return to the OR occurs. In the case of arterial
compromise, immediate return to the OR for
exploration is warranted.
When returning to the OR for exploration and
possible revision, careful inspection of the entire
ap and vascular pedicle is warranted, often
necessitating ap takedown to accomplish this
(Fig.6.6a), and the cause of the vascular complication should be identied. Ensure that there are
no kinks or twists in the pedicle and that the
pedicle is not being externally compressed by
surrounding tissues or hematoma. Once external
causes are excluded, internal causes such as
vasospasm, issues with the anastomosis, or
thrombosis may be the culprit. If venous thrombosis is noted (Fig.6.6b), opening of the anastomosis is warranted with mechanical
thrombectomy either by way of milking out the
clot manually (Fig.6.7) or via Fogarty catheter
(Fig.6.8), irrigation with heparinized saline, cutback of thrombosed segment (with or without
vein grafting as needed), and revision either with
the same vein or another carefully selected
recipient vein. In a comparison of 21 compromised aps with thrombosis of either the venous
or the arterial systems, the use of a Fogarty catheter for mechanical thrombectomy resulted in a
57% rate of successful ap salvage [62]. Risks
of this technique however include further propagation of the thrombus, microtrauma to the ves-
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Fig. 6.7 Manual
removal of venous
thrombosis
Fig. 6.8 Thrombectomy
with Fogarty catheter
N. Patel et al.
sel with possible intimal damage and dissection,
vessel perforation, or device complications such
as rupture or avulsion within the vessel [63].
Thrombolytics such as recombinant tissue plasminogen activator (Rt- PA) in conjunction with
mechanical thrombectomy as a multimodal
approach has also been used and has shown
some promising improvements in ap salvage
rates [64]. The debate on the use of one versus
two venous anastomoses has been an ongoing
one; on the one hand, two veins provide increased
drainage and theoretically less risk of venous
congestion, whereas single venous anastomosis
reduces operating time and allows for easier ap
inset [65]. Xu etal. [66] have reported that the
use of one-vein anastomosis had signicantly
higher salvage rates and earlier time to detection
of ap compromise than two-vein anastomoses
in a cohort of 389 free aps. Despite this, some
studies have demonstrated no difference between
the two [67], and some have shown that two
veins are better than one in reducing the incidence of take- backs and failure rates [68, 69].
Good arterial pulsations should be present and
might be weak or absent in the case of arterial
thrombosis. In this case, takedown of the arterial
anastomosis is warranted with removal of thrombus and cutback to healthy vessel prior to reanastomosis, or selection of another donor artery. If a
length discrepancy or vessel caliber mismatch is
present, consideration should be made to perform vein grafting and/or selection of a new
donor artery. Systemic antithrombotic agents
such as intravenous heparin in doses of 3000 or
5000 units at the time of venous or arterial
reanastomosis may be employed in conjunction,
particularly if thrombus formation rapidly reoccurs at the time of exploration and revision. If a
venous coupler was used, surgeons can use the
same size coupler or a larger one if proper anastomosis can be accomplished. To deal with vascular spasms, the pedicle can be irrigated with
papaverine (alkaloid antispasmodic) to decrease
the incidence of vascular spasm, the ap can be
warmed, and the use of lidocaine and nicardipine
has also been described [70].
Patients demonstrating a history of hyperco-
agulability (antiphospholipid syndrome, factor
6 Free Flap Considerations andComplications
105
V Leiden, factor C and S deciency, etc.) have
demonstrated increased rates of both arterial
and venous thrombosis in free ap surgery [71,
72]. Moreover, patients with malignancies,
which is a major indication for free ap reconstruction in the head and neck, have been shown
to be hypercoagulable at baseline and thus are
inherently at increased risk of thrombosis [73].
Additionally, patients who are treated intraoperatively and/or postoperatively with heparin
are susceptible to thrombosis due to a rare side
effect, heparin- induced thrombocytopenia and
thrombosis (HITT), which can occur in about
0.1–1% of heparinized patients, with higher
rates in patients receiving unfractionated heparin (UFH) as compared to low-molecular-weight
heparin (LMWH) [74–76]. These patients
should be switched to a non-heparin anticoagulant such as argatroban and likely will require
long-term coumadin therapy. Patients who have
repeated clotting, either intraoperatively or
postoperatively, should have a hypercoagulability workup to determine if a thrombophilic disorder is present. Once successful ap salvage
has been achieved, postoperative care becomes
a vital component of maintenance of a healthy
ap. Close observation of the ap within an
intensive care unit (ICU) with trained personnel
becomes vital, with careful attention to neck
position to prevent kinking, twisting, or stretching of the vessels, as well as close monitoring of
vitals, laboratory values, and overall patient status. Education of ICU staff on ap monitoring is
crucial to ensure adequate care and early recognition of problematic issues. There currently
exists a paucity of data and evidence- based
research regarding the use of therapeutic anticoagulation after successful free ap salvage.
Senchenkov etal. looked at a large series of 395
free aps for breast reconstruction and advocated for routine postoperative anticoagulation
with heparin in all patients who experienced
both intraoperative and postoperative thrombotic events, with the addition of antiplatelet
therapy for those with repeated thromboses.
However, targeted protocols in this scenario in
head and neck reconstructive surgery have not
yet been established [77].
While surgical exploration and revision of
compromised aps remain the mainstay of management for these patients, there exist situations
in which other options must be explored. In cases
where the patient may be too unstable to return to
the OR, or where thromboses are too numerous
or too distal to warrant access and revision, or in
case of repeated clotting, nonsurgical options are
to be considered. These can include the use of
thrombolytics, anticoagulants, hyperbaric oxygen therapy (HBOT), or medicinal leeches
(Hirudo medicinalis).
The use of Rt-PA has been described in the
literature for salvage of venous congested free
aps. Rt-PA is a thrombolytic that encourages the
conversion of plasminogen to plasmin and initiates local brinolysis, thus aiding in the resolution of venous and arterial clotting. Not all
patients are candidates for thrombolytic therapy,
however, as patients with a history of bleeding
diatheses and patients who are at high risk of
intracranial, gastrointestinal, and other bleeds
may represent absolute contraindications to this
therapy. Tran etal. [78] have previously described
successful use of subcutaneous injection of
Rt-PA directly into aps, with return of capillary
rell and resolution of venous congestion. Often,
this is not employed as a rst option; however,
after multiple attempts at venous revision, this
becomes a consideration. Ayhan et al. [79]
employed the use of Rt-PA after three attempts at
venous anastomosis with recurrent venous congestion, where injection of 2 mg of Rt-PA into
multiple areas of their aps allowed for successful salvage. Ihler et al. [80] reported return of
capillary rell between 4 and 8h after injection,
though this can vary depending on ap size and
varying severity of ap thrombosis. Additionally,
the use of thrombolytic therapy intra-arterially
for ap salvage in the case of venous congestion
was rst described in 1987 by Lipton and Jupiter
and is well described and utilized today [81–84].
This may help not only with thrombosis at the
level of the pedicle, but also with clotting within
the microcirculation of the ap itself, as this can
be a signicant cause of ap failure.
The use of heparin to relieve venous congestion
was rst described in 1989 in cases of digital
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