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N. Patel et al.
replantation [85], and the use of LMWH has been
described in salvage of free aps. Injection of
LMWH directly into areas of the congested ap in
a subcutaneous fashion has been described, with
the onset of action and time to visible effect
reported to be about 2h, with peak effect occurring
at about 4–5 h and duration of effect of about
12–24 h. It has been recommended that doses of
20–40mg every 4–6h should be implemented for
the rst 1–3days, decreasing to 10–20mg every
24 h around the 10–14-day mark [86]. Therapy
should be continued for a minimum of 10days, as
studies have identied the time frame for the reestablishment of neovascularization to be around
7–10days [87]. As with Rt-PA, the use of LMWH
can be useful in cases of thrombosis both at the
level of the pedicle and within the microcirculation
of the ap, which may not be amenable to surgical
exploration. In addition to its anticoagulant effects,
heparin has been shown to reduce endothelial dysfunction within the microcirculation of postischemic aps, thus providing a protection against
reperfusion injury that is independent of its systemic anticoagulant effects, though the exact mechanism of this effect is yet unknown. It has been
postulated to be linked to effects such as inhibition
of leukocyte adhesion to postischemic endothelium
via increases in nitric oxide synthesis, reduction of
free radicals due to its capacity to release superoxide dismutase from the endothelium, as well as
direct anti-inammatory effects [88–90].
Leeches (hirudotherapy) have shown promise
in the management of venous congested aps,
particularly as a bridge to formal surgical exploration and revision [91, 92]. Leech therapy is
only useful, however, in cases where arterial
inow is patent and sufcient, and therapy is targeted at decreasing the accumulating venous
pressure within the ap (Fig. 6.9). Leeches
secrete a non-heparin anticoagulant called hirudin, which aids in the feeding process. Leeches
are kept in refrigerated distilled water with
Hirudo salt. Prior to application, any blood clots
should be cleaned off with dry gauze (use of alcohol swabs may interfere with latching). The leech
is grasped with gloves or non-toothed forceps
and placed onto the ap. If the leech does not
latch, the ap can be pricked to induce bleeding
to encourage the leech to latch. The leech will
generally detach once it is fully distended and
must be monitored to prevent migration of the
leech to other areas, with treatment lasting anywhere from 30 min to 4–5 h. Leeches are then
euthanized in 70% isopropyl alcohol and discarded. All patients are placed on antibiotics prophylaxis for Aeromonas hydrophila for the
duration of leech therapy, which consists of doxycycline, ciprooxacin, ceftriaxone, or Bactrim,
with prophylaxis continuing for 14 days after
cessation of leech therapy. Furthermore, the
patient’s hemoglobin levels must be monitored
throughout the treatment period every 6h, and
transfusion should be considered if levels drop
below 10g/dL in symptomatic patients [93]. It
should be noted that leech therapy has not been
shown to help salvage all venous congested tissues and as such should not be used as a primary
method of ap salvage [94, 95].
HBOT has been shown to improve the survival of free ap failures in the setting of arterial,
venous, and combined arteriovenous insufciency; however, it has been validated primarily
in animal models [96]. In contrast to leech therapy, HBOT has been shown to impact ap survival greatest in cases of arterial insufciency,
secondary to its ability to enhance broblasts and
collagen synthesis, promote neovascularization,
and reduce local hypoxic insults [97, 98]. Further
Fig. 6.9 Use of
medicinal leeches on
venous congested ap.
Note the improvement
of central portion of
ap, with necrosis of
limited to lateral edge
and distal tip
6 Free Flap Considerations andComplications
107
investigation in human subjects is necessary at
this time to better evaluate the efcacy of HBOT
as an accepted mode of free ap salvage in head
and neck reconstructive surgery.
Hematomas
The formation of hematomas not only compromises tissues by the extrinsic pressure effect they
elicit, but they also induce a complex sequence of
interrelated biochemical and cellular events,
including neutrophil inltration, cytokinemediated inammation, and a prothrombotic
state, which leads to synthesis of reactive oxygen
species and activation of the complement system,
resulting in tissue injury, as well as vascular
thrombosis [99, 100]. Sources of bleeding may
include the vascular pedicle, tissue bed, as well
as bleeding from ap edges. Postoperative
hematoma formation (Fig. 6.10) accounts for
anywhere between 0.2% and 30% [101] of postoperative complications relating to free aps in
head and neck reconstruction, representing the
second most common postoperative complication in free aps, just behind vascular thrombosis
[102]. This is higher than other regions of the
body, likely relating to increased dead space in
the head and neck with more anatomical constraints, more complex vascular anatomy, as well
as difculty in immobilization and autonomic
reexes such as gagging and coughing, as well as
vomiting, resulting in inadvertent pedicle disruption or vascular leakage [103]. Studies have
shown that free aps are compromised by hematomas 2–4% of the time within this cohort, most
commonly resulting from compromise of venous
outow and ap congestion [104]. As such, early
recognition of hematoma formation and management are crucial to free ap salvage. A study by
Chen etal. concluded that if return to the OR for
re-exploration and salvage was within 36h, salvage rates were signicantly higher at 84% as
compared to 50% if return to OR was after this
time frame, with salvage rates especially higher
in cases where there was an absence of thrombosis [105]. Other studies have shown salvage rates
of 93.3% if return to OR was within 5h of detection, and 100% in the absence of thrombosis, as
compared to 58.3% in the presence of vascular
thrombosis [106]. The use of postoperative anticoagulation to decrease vascular thrombosis rates
in free aps remains a debated topic with no consensus as of yet. Studies have shown that in cases
where no anticoagulation therapy was used, rates
of free ap failure, thrombosis, as well as rates of
hematoma formation were similar to rates of various anticoagulation therapies [107, 108].
However, a study by Kroll etal. demonstrated a
statistically signicant increase in rates of hematoma formation in patients who received highdose heparin for pedicle thrombosis prophylaxis
at 20% [109]. Moreover, other studies have
shown that the use of NSAIDs postoperatively
has been associated with higher rates of hematoma formation in this cohort, with aspirin showing the lowest rates of hematomas [110, 111]. All
this may suggest that anticoagulation postoperatively offers no or minimal improvement in ap
survival and minimal effect on ap-related complications in the postoperative setting [112].
Despite this, patients often require chemoprophylaxis for reasons other than prevention of ap
thrombosis, such as prevention of VTE, and thus
Fig. 6.10 Formation of
postoperative
hematomas in free ap
patients
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N. Patel et al.
this should be taken into consideration. It has
also been suggested that postoperative blood
pressure control can inuence rates of hematoma
formation and should ideally be <150 mmHg
systolic, as rates of hematoma formation can
increase with even transient increases of about
165mmHg systolic [113]. Despite this, maintaining a high enough blood pressure to maintain
good ap perfusion and avoiding signicant periods of hypotension are essential, with systolic
blood pressure ideally maintained above
100mmHg for this purpose [114].
Signs of the presence of a hematoma can
sometimes be subtle, with just the localized
development of ecchymosis in the cervical region
or just the presence of a mild amount of edema.
Other times, evidence of hematoma formation is
more obvious, with the presence of a large swelling, ecchymosis, bleeding from between sutures,
compression of the vascular pedicle, and venous
outow blockage.
One method by which to manage hematoma
formation is the removal of sutures at bedside
with evacuation of the hematoma. Some authors
however have stated that given the cytotoxic
nature of the effects of a hematoma, as well as the
potential for incomplete hematoma evacuation,
performing this maneuver is not sufcient and
return to the OR for exploration and formal evacuation is recommended (Fig. 6.11) [115].
Additionally, formal exploration is often warranted in order to identify and obtain surgical
control of bleeders if present, and to examine the
vascular pedicle for potential thrombosis. If reexploration is performed prior to the formation of
vascular thrombosis, salvage rates are signicantly higher, underscoring the importance of
early detection.
Salvage Reconstruction
Unfortunately, there are the rare instances where
ap salvage appears to be unlikely, and surgeons
are left to make a tough decision, namely when to
terminate salvage efforts and what steps to take
next. In the case of partial ap failure, options for
management depend primarily on the amount of
residual defect after partial ap debridement or
excision, location of the defect, as well as tissue
availability. In cases where a small defect
remains, local tissue rearrangement sometimes
sufces for the purposes of wound coverage,
whereas larger defects may necessitate the use of
a regional ap. If the defect involves a communication of the oral cavity to the neck, salivary leak
into the cervical tissues becomes a signicant
consideration, given the increased risk of infection and stula formation. In the setting of total
ap failure, one must balance the needs of the
wound or defect for reconstruction with a goal of
restoring form and function, with the ability of
the patient to tolerate another extensive procedure and to decide what additional procedure
should be undertaken. The reconstructive options
remain similar, a second free tissue transfer,
regional ap, or local tissue rearrangement
(Fig.6.12) [4]. In addition to the tolerance of a
secondary procedure, consideration should be
made for extended hospital stay with potential for
Fig. 6.11 Complete
evacuation of hematoma
during exploratory
surgery in OR
6 Free Flap Considerations andComplications
109
Fig. 6.12 Unsalvageable necrotic free ap with removal of ap, and salvage supraclavicular ap performed for cheek
reconstruction
110
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Fig. 6.12 (continued)
additional morbidity, as well as the timing of
radiation, if applicable, as a delay in this treatment modality is not favorable. The decision of
what type of secondary reconstruction should be
done at this time depends on several factors,
including the type and location of the original
defect, number and amount of available tissues or
ap options, and patient comorbidities and stability. The simplest reconstruction should be undertaken, one that has the highest chance of success
and the minimum amount of additional patient
morbidity. For example, in the case of maxillomandibular reconstruction with a free osteocutaneous bula ap, in the event of bula ap failure,
the ideal salvage ap would be a second free bula ap, as that has the highest chance of meeting
the reconstructive requirements. However, if a
second bula ap cannot be harvested due to anatomic restrictions (lack of adequate three-vessel
runoff), or due to the patient’s fragility or inability to tolerate a second lengthy procedure, one
should consider a soft tissue ap such as an
anterolateral thigh ap or radial forearm free ap
to obtain wound coverage, which would provide
a shorter procedure and thus less morbidity for
the patient. If the patient will be obtaining dental
implants, secondary bone grafting can be considered at a later stage. Another option in this case
can be a pedicled ap, such as a pectoralis myocutaneous ap if the surgeon chooses to avoid
N. Patel et al.
another free ap procedure because of a vesseldepleted neck, patient stability issues, diagnosis
of thrombophilic disorder, severe infection, etc.
Salvage reconstruction often presents a challenge
as it occurs in a previously operated wound bed,
often contaminated or infected, and the ideal ap
has already been utilized. As such, success rates
in the salvage setting often drop as compared to
the primary reconstruction setting. Bozikov and
Arnez found that ap failures in the salvage operation were 4.6× more likely, with a success rate
of only 53.3% [116]. Salvage reconstruction can
be done either in the immediate setting or in a
delayed fashion, depending on these factors,
though most surgeons will opt to perform it
immediately. In the head and neck, this presents a
particular challenge as specic issues come into
consideration, such as dealing with vesseldepleted necks, salivary contamination/leak if a
composite defect of the oral cavity is involved,
patients having a history of prior radiation,
patients with head and neck cancer who are often
malnourished with poor wound healing, and need
for coverage of the great vessels, among others
[117]. In cases of limited availability of adequate
vessels for anastomosis, due to radiation damage
or depletion from previous free ap surgery, surgeons can consider options such as vein grafting;
use of the internal mammary, thoracoacromial
vessels, or transverse cervical vessels; and use of
the contralateral neck vessels, or end-to-side
anastomoses, in particular with the internal jugular vein, as this provides reliable drainage, good
caliber, and consistent anatomy [118–121].
Though surgeons often desire to provide patients
with the best reconstructive option possible, one
must also consider that sometimes the best reconstruction … is no reconstruction. The use of synthetic prostheses, when available, often can
represent excellent alternatives as prosthetic
reconstruction, for patients in whom surgical
reconstruction is not an option. A wide variety of
options exist for orbital, nasal, maxillary, and
auricular reconstruction, with or without implants
for support and retention [122].
6 Free Flap Considerations andComplications
111
Conclusion
Free ap reconstruction of the head and neck represents a complex surgical endeavor and can be
wrought with complications at any stage of
patient care. Surgeons must be mindful and must
employ careful patient selection and workup, as
well as demonstrate excellent surgical technique,
and patients should be carefully and constantly
monitored in the immediate postoperative period
to help mitigate, and ideally avoid, these complications. Surgeons must be adept at recognizing
issues early that could potentially compromise
ap viability and be prepared to perform additional salvage procedures to maximize success
rates.
References
1. Wax MK. The role of the implantable Doppler
probe in free ap surgery. Laryngoscope.
2014;124:S1–S12.
2. Cervenka B, Bewley AF. Free ap monitoring: a
review of the recent literature. Curr Opin Otolaryngol
Head Neck Surg. 2015;23:393–8.
3. Corbitt C, Skoracki RJ, Yu P, Hanasono M.Free ap
failure in head and neck reconstruction. Head Neck.
2014;36(10):1140–5.
4. Wei FC, Demirkan F, Chen FC. The outcome of
failed free aps in head and neck and extremity
reconstruction: what is next in the reconstructive
ladder? Plast Reconstr Surg. 2001;108(5):1154–62.
5. Chim H, Salgado CJ, Sesselgyte R, Wei FC, Mardini
S. Principles of head and neck reconstruction: an
algorithm to guide ap selection. Semin Plast Surg.
2010;24(2):148–54.
6. Ishimaru M, Ono S, Suzuki S, Matsui H, Fushimi
K, Yasunaga H.Risk factors for free ap failure in
2,846 patients with head and neck cancer: a national
database study in Japan. J Oral Maxillofac Surg.
2016;74:1260–70.
7. Serletti JM, Higgins JP, Moran S, Orlando
GS.Factors affecting outcome in free-tissue transfer
in the elderly. Plast Reconstr Surg. 2000;106:66–70.
8. Lin Y, He JF, Zhang X, Wang HM. Intraoperative
factors associated with free ap failure in the head
and neck region: a four-year retrospective study of
216 patients and review of the literature. Int J Oral
Maxillofac Surg. 2019;48:447–51.
9. Spiegel JH, Polat JK.Microvascular ap reconstruction by otolaryngologists: prevalence, postoperative
care, and monitoring techniques. Laryngoscope.
2007;117:485–90.
10. Zhou W, Zhang WB, Yu Y, Guo CB.Risk factors for
free ap failure: a retrospective analysis of 881 free
aps for head and neck defect reconstruction. Clin
Paper Reconstruct Surg. 2017;46(8):941–5.
11. Zhang C, Sun J, Zhu H, Xu L, Ji T. Microsurgical
free ap reconstructions of the head and neck region:
Shanghai experience of 34 years and 4640 aps. Int J
Oral Maxillofac Surg. 2015;44:675–84.
12. Kwok AC, Agarwal JP.An analysis of free ap failure using the ACS NSQIP database. Does ap site
and ap type matter? Microsurgery. 2017;37:531–8.
13. Dillon PF, Aksoy MO, Driska SP, Murphy
RA. Myosin phosphorylation and the crossbridge cycle in arterial smooth muscle. Science.
1981;211:495–7.
14. Vargas CR, Iorio ML, Lee BT.A systematic review
of topical vasodilators for the treatment of intraoperative vasospasm in reconstructive microsurgery.
Plast Reconstr Surg. 2015;136:411–22.
15. Hirsch J, Salzman EW, Marder VJ, Colman
RW. Overview of the thrombotic process and its
therapy. Hemostasis and thrombosis, basic principles
and clinical practice. Philadelphia: JB Lippincott
company; 1994. p.1151–64.
16. Haughey BH, Wilson E, Kluwe L, Piccirillo J.Free
ap reconstruction of the head and neck: analysis of 241 cases. Otolaryngol Head Neck Surg.
2001;125:10–7.
17. Ruttmann T, James MF, Finlayson J. Effects on
coagulation of intravenous crystalloid or colloid in
patients undergoing peripheral vascular surgery. Br
J Anaesth. 2002;89:226–30.
18. Brinkman JN, Derks LH, Klimek M, Mureau
MA. Perioperative uid management and use of
vasoactive and antithrombotic agents in free ap
surgery: a literature review and clinical recommendations. J Reconstr Microsurg. 2013;29:357–66.
19. Kelly D, Reynolds M, Crantford C, Pestana I.Impact
of intraoperative vasopressor use in free tissue transfer for head, neck and extremity reconstruction. Ann
Plast Surg. 2014;72(6):S135–8.
20. Gardner JR, Gau V, Page P, Dunlap Q, King
D. Association of continuous intraoperative vasopressor use with reoperation rates in head and neck
free-ap reconstruction. JAMA Otolaryngol Head
Neck Surg. 2021;147(12):1059–64.
21. Roan TL, Lin MH, Lee CH. Microvascular ap
reconstruction after the head and neck tumor resections: a review of 10 years NTUH experience. J Plast
Surg Assoc ROC. 2010;19:199–208.
22. Chiu YH, Chang DH, Perng CK. Vascular complications and free ap salvage in head and neck
reconstructive surgery: analysis of 150 cases of
Reexploration. Ann Plast Surg. 2017;78:S83–8.
23. Trussler AP, Watson JP, Crisera CA. Late freeap salvage with catheter-directed thrombolysis.
Microsurgery. 2008;28:217–22.
24. Tse R, Ross D, Gan BS. Late salvage of a free
TRAM ap. Br J Plast Surg. 2003;56:59–62.
112
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
N. Patel et al.
25. Genden EM, Rinaldo A, Suarez C, Wei WI, Bradley
PJ, Ferlito A. Complications of free ap transfers
for head and neck reconstruction following cancer
resection. Oral Oncol. 2004;40:979–84.
26. Wong CH, Wei FC. Microsurgical free ap
in head and neck reconstruction. Head Neck.
2010;32:1236–45.
27. Chang EI, Zhang H, Liu J.Analysis of risk factors
for ap loss and salvage in free ap head and neck
reconstruction. Head Neck. 2016;38:E771–5.
28. Selber JC, Angel Soto-Miranda M, Liu J, Robb
G. The survival curve: factors impacting the outcome of free ap takebacks. Plast Reconstr Surg.
2012;130:105–13.
29. Yu P, Chang DW, Miller MJ, Reece G. Analysis
of 49 cases of ap compromise in 1310 free aps
for head and neck reconstruction. Head Neck.
2009;31:45–51.
30. Hillberg NS, Beugels J.Increase of major complications with a longer ischemia time in breast reconstruction with a free deep inferior epigastric perforator
(DIEP) ap. Eur J Plast Surg. 2020;43:133–8.
31. Angel MF, Knight KR, Amiss LR, Morgan
RF. Further investigation of secondary venous
obstruction. Microsurgery. 1992;13(5):255–7.
32. Hjortdal VE, Sinclar T, Kerrigan CL, Solymoss
S. Venous ischemia in skin aps: microcirculatory intravascular thrombosis. Plast Reconstr Surg.
1994;93:366–74.
33. Angel MF, Knight KR, Mellow CG, Wanebo
J. Timing relationships for secondary ischemia in
rodents: the effect of venous obstruction. J Reconstr
Microsurg. 1992;8:107–9.
34. Stotland MA, Kerrigan CL.The role of platelet activating factors in musculocutaneous ap perfusion
injury. Plast Reconstr Surg. 1997;99:1989–99.
35. Carroll WR, Esclamado RM. Ischemia/reperfusion injury in microvascular surgery. Head Neck.
2000;22:700–13.
36. Ammes A, Wright RL, Kowada M, Thirsten JM,
Majno G.Cerebral ischemia II: the no re-ow phenomenon. Am J Pathol. 1968;52:437–53.
37. Chen KT, Mardini S, Chuang DC. Timing of presentation of the rst signs of vascular compromise
dictates the salvage outcome of free ap transfers.
Plast Reconstr Surg. 2007;120:187–95.
38. Ho MW, Brown JS, Magennis P.Salvage outcomes
of free tissue transfer in Liverpool: trends over 18
years (1992–2009). Br J Oral Maxillofac Surg.
2012;50:13–8.
39. Bui DT, Cordeiro PG, Hu QY.Free ap reexploration:
indications, treatment, and outcomes in 1193 free
aps. Plast Reconstr Surg. 2007;119:2092–100.
40. Disa JJ, Cordeiro PG, Hilgado DA.Efcacy of conventional monitoring techniques in free tissue transfer: an 11-year experience in 750 consecutive cases.
Plast Reconstr Surg. 1999;104:97–101.
41. Betancourt FM, Mah ET, McCabe SJ. Timing of
critical thrombosis after replantation surgery of the
digits. J Reconstr Microsurg. 1998;14:313–6.
42. Salgado CJ, Smith A, Kim S. Effects of late loss
of arterial inow on free ap survival. J Reconstr
Microsurg. 2002;18:579–83.
43. Khoo CTK, Bailey BN. The behaviour of free
muscle and musculocutaneous flaps after early
loss of axial blood supply. Br J Plast Surg.
1982;35:43–6.
44. Clarke HM, Chen G.Peripheral neovascularization
of muscle and musculocutaneous aps in the pig.
Plast Reconstr Surg. 1992;89:109–13.
45. Black MJM, Chait L, OBrien BM, Sykes PJ.How
soon may the axial vessels of a surviving free ap
be safely ligated: a study in pigs. Br J Plast Surg.
1978;31:295–9.
46. Ceulemans P, Landuyt KV, Hamdi M, Blondeel
P.Complete survival of a free ap after early pseudoaneurysm formation and pedicle thrombosis. Ann
Plast Surg. 2001;47:332–5.
47. Rothaus KO, Acland RD. Free ap neovascularization: case report. Br J Plast Surg.
1983;36:348–9.
48. Ribuffo D, Chiummariello S, Cigna E, Scuderi
N. Salvage of a free ap after late total thrombosis of the ap and revascularization. Scand J Plast
Reconstr Hand Surg. 2004;38:50–2.
49. Machens HG, Pallua N, Pasel J, Mailaender
P. Persistence of pedicle blood ow up to 10 years
after free musculocutaneous tissue transfer. Plast
Reconstr Surg. 1998;101:719–26.
50. Sadove RC, Kanter MJ. Absent neovascularization in a lower extremity free ap: a case report. J
Reconstr Microsurg. 1993;9:5–9.
51. Kumar K, Jaffe W, London NJ, Varma SK. Free
ap neovascularization: myth or reality? J Reconstr
Microsurg. 2004;20:31–4.
52. Kadota H, Sakuraba M, Kimata Y. Analysis of
thrombosis on postoperative day 5 or later and
microvascular reconstruction for head and neck cancers. Head Neck. 2009;31:635–41.
53. Chachques JC, Mitz V, Zapata R. Risk of consequence of infection at the site of microsurgical
repair: an experimental model. Ann Plast Surg.
1986;17:221–7.
54. De Vries EJ, Myers EN, Johnson JT.Jejunal interposition for repair of stricture or stula after laryngectomy. Ann Otol Rhinol Laryngol. 1990;99:496–8.
55. Sweeny L, Topf M, Wax MK. Shift in the timing of microvascular free tissue transfer failures
in head and neck reconstruction. Laryngoscope.
2020;130:347–53.
56. Novakovic D, Patel RS, Goldstein DP, Gullane
PJ.Salvage of failed free aps used in head and neck
reconstruction. Head Neck Oncol. 2009;1:33.
57. Wu CC, Lin PY, Chew KY. Free tissue transfers
in head and neck reconstruction: complications,
outcomes and strategies for management of ap
failure: analysis of 2019 Flaps in single institute.
Microsurgery. 2014(34):339–44.
58. Pohlenz P, Klatt J, Schon G. Microvascular free
aps in head and neck surgery: complications and
6 Free Flap Considerations andComplications
113
outcome of 1000 aps. Int J Oral Maxillofac Surg.
2012;41:739–43.
59. Fukuiwa T, Nishimoto K, Hayashi T, Kurono
Y.Venous thrombosis after microvascular free- tissue
transfer in head and neck cancer reconstruction.
Auris Nasus Larynx. 2008;35(3):390–6.
60. Hanasono MM, Butler CE.Prevention and treatment
of thrombosis in microvascular surgery. J Reconstr
Microsurg. 2008;24(5):305–14.
61. May JW Jr, Chait LA, O’Brien BM. The no-reow
phenomenon in experimental free aps. Plast
Reconstr Surg. 1978;61:256–67.
62. Troeltzsch M, Troeltzsch M, Probst FA. Current
concepts in salvage procedures for failing microvascular aps: is there a superior technique? Insights
from a systematic review of the literature. Int J Oral
Maxillofac Surg. 2016;45:1378–87.
63. Khansa I, Chao AH, Taghizadeh M. A systematic
approach to emergent breast free ap takeback:
clinical outcomes, algorithm, and review of the literature. Microsurgery. 2013;33:505–13.
64. Brouwers KKA. Management of free ap salvage
using thrombolytic drugs: a systematic review. J
Plast Reconstr Aesthet Surg. 2020;73:1806–14.
65. Han Z, Li J, Li H.Single versus dual venous anastomoses of the free bula osteocutaneous ap in
mandibular reconstruction: a retrospective study.
Microsurgery. 2013;33:652–5.
66. Xu Z, Zhao XP, Yan TL. A 10-year retrospective study of free anterolateral thigh ap application in 872 head and neck tumour cases. Int J Oral
Maxillofac Surg. 2015;44:1088–94.
67. Boczar D, Colon RR, Chaya BF.Are two veins better than one in free ap head and neck reconstruction? Plast Reconstr Surg. 2021;9(10S):63–4.
68. Chen WF, Kung YP, Kang YC. An old controversy revisited-one versus two venous
anastomoses in microvascular head and neck reconstruction using anterolateral thigh ap. Microsurgery.
2014;34(5):377–83.
69. Riot S, Herlin C, Mojallal A. A systematic review
and meta-analysis of double venous anastomosis in
free aps. Plast Reconstr Surg. 2015;136:1299–311.
70. Egozi D, Fodor L, Ullmann Y. Salvage of compromised free aps in trauma cases with combined
modalities. Microsurgery. 2011;31:109–15.
71. Salgarello M, Cervelli D, Barone-Adesi L.A massive arterial thrombosis of a free anterolateral thigh
ap in a patient with antiphospholipid syndrome.
Microsurgery. 2008;28:447–51.
72. Ayala C, Blackwell KE. Protein C deciency
in microvascular head and neck reconstruction.
Laryngoscope. 1999;109:259–65.
73. Olsson E, Svartling N, Asko-Seljavaara S, Lassila
R.Activation of coagulation and brinolysis during
reconstructive microsurgery in patients with cancer.
Microsurgery. 2001;21:208–13.
74. Segna E, Bolzoni AR, Beserga C. Free ap loss
caused by heparin-induced thrombocytopenia and
thrombosis (HITT): a case report and literature
review. Acta Otorhinolaryngol Ital. 2016;36:527–33.
75. Tremblay DM, Harris PG, Gagnon AR. Heparininduced thrombocytopenia syndrome as a cause of
ap failure: a report of two cases. J Plast Reconstr
Aesthet Surg. 2008;61:78–83.
76. McCleave MJ.Free ap failure caused by heparininduced thrombocytopenia. Microsurgery.
2010;30:251–2.
77. Senchenkov A, Lemaine V, Tran NV.Management
of perioperative microvascular thrombotic complications- the use of multiagent anticoagulation algorithm in 395 consecutive free aps. J Plast Reconstr
Aesthet Surg. 2015;68:1293–303.
78. Tran NV, Bishop AT, Convery PA, Yu AY. Venous
congestive ap salvage with subcutaneous
Rt-PA.Microsurgery. 2006;26:370–2.
79. Ayhan S, Uygur S, Kucukoduk I, Sencan A.Salvage
of a congested DIEAP ap with subcutaneous
recombinant tissue plasminogen activator treatment.
J Plast Reconstr Aesthet Surg. 2009;62:e453–4.
80. Ihler F, Matthias C, Canis M. Free ap salvage
with subcutaneous injection of tissue plasminogen
activator in head and neck patients. Microsurgery.
2013;33:478–81.
81. Panchapakesan V, Addison P, Beausang E, Lipa
JE. Role of thrombolysis in free-ap salvage. J
Reconstr Microsurg. 2003;19:523–30.
82. Yii NW, Evans GR, Miller MJ, Reece
GP. Thrombolytic therapy: what is its role in free
ap salvage? Ann Plast Surg. 2001;46:601–4.
83. Chang EI, Mehrara BJ, Festekjian JH. Vascular
complications and microvascular free ap salvage:
the role of thrombolytic agents. Microsurgery.
2011;31:505–9.
84. Casey WJ, Craft RO, Rebecca AM, Smith
AA. Intraarterial tissue plasminogen activator: an
effective adjunct following microsurgical venous
thrombosis. Ann Plast Surg. 2007;59:520–5.
85. Barnett GR, Taylor GI, Mutimer KL. The “chemical leech”: intra-replant subcutaneous heparin as an
alternative to venous anastomosis. Report of three
cases. Brit J Plast Surg. 1989;42(5):556–8.
86. Perez M, Sancho J, Ferrer C.Management of ap
venous congestion: the role of heparin local subcutaneous injection. J Plast Reconstr Aesthet Surg.
2014;67:48–55.
87. Seran D, Shearin JC, Georgiade NG.The vascularization of free aps: a clinical and experimental
correlation. Plast Reconstr Surg. 1977;60:233–41.
88. Ma XL, Weyrich AS, Lefer DJ.Diminished basal
nitric oxide release after myocardial ischemia and
reperfusion promotes neutrophil adherence to the
coronary endothelium. Circ Res. 1993;72:403–12.
89. Li JM, Hajarizadeh H, LaRosa CA. Heparin and
protamine stimulate the production of nitric oxide. J
Cardiovasc Surg. 1996;37:445–52.
90. Oyunagui Y, Sato S. Heparin, a potent releasing agent of extracellular superoxide dismutase
(EC-SOD) suppresses paw oedema in mice. Free
Radic Res Commun. 1990;9:87–99.
91. Hayden RE, Phillips JG, McLear PW. Leeches:
objective monitoring of altered perfusion in
114
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
N. Patel et al.
congested aps. Arch Otolaryngol Head Neck Surg.
1988;114:1395–9.
92. Chepeha DB, Nussenbaum B, Bradford CR.Leech
therapy for patients with surgically unsalvageable
venous obstruction after revascularized free tissue transfer. Arch Otolaryngol Head Neck Surg.
2002;128:960–5.
93. Koch CA, Olsen SM, Moore EJ.Use of the medicinal
leech for salvage of venous congested microvascular
free aps of the head and neck. Am J Otolaryngol
Head Neck Med Surg. 2012;33:26–30.
94. Akyurek M, Safak T, Kecik A. Microsurgical ear
replantation without venous repair: failure of development of venous channels despite patency of
arterial anastomosis for 14 days. Ann Plast Surg.
2001;46:439–42.
95. Miller PJ, Hertler C, Alexiades G. Replantation of
the amputated nose. Arch Otolaryngol Head Neck
Surg. 1998;124:907–10.
96. Friedman HI, Fitzmaurice M, Lefaivre JF. An
evidence-based appraisal of the use of hyperbaric
oxygen on aps and grafts. Plast Reconstr Surg.
2006;117(7):175–90.
97. Helmers R, Milstein DM, van Hulst RA, de Lange
J.Hyperbaric oxygen therapy accelerates vascularization in keratinized oral mucosal surgical aps.
Head Neck. 2014;36:1241–7.
98. Bill TJ, Hoard MA, Gampper TJ.Applications of
hyperbaric oxygen in otolaryngology head and neck
surgery: facial cutaneous aps. Otolaryngol Clin N
Am. 2001;34:753–66.
99. Kucur C, Durmus K, Uysal IO. Management of
complications and compromised free aps following major head and neck surgery. Eur Arch
Otorhinolaryngol. 2016;273:209–13.
100. Khouri RK, Cooley BC, Kunselman AR.A prospective study of microvascular free ap surgery and outcome. Plast Reconstr Surg. 1998;102:711–21.
101. Schusterman MA, Miller MJ, Reece GP, Kroll
SS.A single center’s experience with 308 free aps
for repair of head and neck cancer defects. Plast
Reconstr Surg. 1994;93:472–8.
102. Nakatsuka T, Harii K, Asato H.Analytic review of
2372 free ap transfers for head and neck reconstruction following cancer resection. J Reconstr
Microsurg. 2003;19:363–8.
103. Tan BK, Por YC, Chen HC. Complications of head
and neck reconstruction and their treatment. Semin
Plast Surg. 2010;24:288–98.
104. Brown JS, Devine JC, Magennis P. Factors
that influence the outcome of salvage in free
tissue transfer. Br J Oral Maxillofac Surg.
2003;41:16–20.
105. Chen YF, Wang TH, Chiu YH.Postoperative hematoma in microvascular reconstruction of the head
and neck. Ann Plast Surg. 2018;80:15–20.
106. Ahmad FI, Gerecci D, Gonzalez JD, Wax MK.The
role of postoperative hematoma on free ap compromise. Laryngoscope. 2015;125:1811–5.
107. Lighthall JG, Cain R, Ghanem TA, Wax MK.Effect
of postoperative aspirin on outcomes in microvas-
cular free tissue transfer surgery. Otolaryngol Head
Neck Surg. 2013;148:40–6.
108. Riva FM, Chen YC, Tan NC. The outcome of
prostaglandin-E1 and dextran-40 compared to no
antithrombotic therapy in head and neck free tissue
transfer: analysis of 1,351 cases in a single center.
Microsurgery. 2012;32:339–43.
109. Kroll SS, Miller MJ, Reece GP.Anticoagulants and
hematomas in free ap surgery. Plast Reconstr Surg.
1995;96:643–7.
110. Kaplan ED, RozenWM SR. Preventing postoperative haematomas in microvascular reconstruction of
the head and neck: lessons learnt from 126 consecutive cases. ANZ J Surg. 2008;78:383–8.
111. Dhiwakar M, Khan NA, McClymont LG. Surgical
resection of cutaneous head and neck lesions:
does aspirin use increase hemorrhagic risk? Arch
Otolaryngol Head Neck Surg. 2006;132:1237–41.
112. Swartz JE, Aarts MC, Swart KM.The value of postoperative anticoagulants to improve ap survival in
the free radial forearm ap: a systematic review and
retrospective multicentre analysis. Clin Otolaryngol.
2015;40:600–9.
113. Wang KY, Yang KC, Su FY, Chen YC. Association
between blood pressure and postoperative
Hematomas in the patients undergoing head and neck
cancer reconstruction. Head Neck. 2019;41:3241–6.
114. Schrey A, Kinnunen I, Vahlberg T.Blood pressure
and free ap oxygenation in head and neck cancer
patients. Acta Otolaryngol. 2011;131:757–63.
115. Glass GE, Nanchahal J. Why haematomas cause
ap failure: an evidence-based paradigm. J Plast
Reconstr Aesthet Surg. 2012;65:903–10.
116. Bozikov K, Arnez ZM. Factors predicting free ap
complications in head and neck reconstruction. J
Plast Reconstr Aesthet Surg. 2006;59:737–42.
117. Bender-Heine A, Sweeny L, Curry JM, Petrisor
D.Management of the Acute Loss of a free ap to
the head and neck—a multi-institutional review.
Laryngoscope. 2021;131:518–24.
118. Halvorson EG, Cordeiro PG, Halvorson EG.Go for
the jugular: a 10-year experience with end-to-side
anastomosis to the internal jugular vein in 320 head
and neck free aps. Ann Plast Surg. 2007;59:31–5.
119. Yamamoto Y, Nohira K, Kuwahara H, Sekido
M.Superiority of end-to-side anastomosis with the
internal jugular vein: the experience of 80 cases in
head and neck microsurgical reconstruction. Br J
Plast Surg. 1999;52:88–91.
120. Aycock JK, Stenson KM, Gottlieb LJ. The thoracoacromial trunk: alternative recipient vessels in
reoperative head and neck reconstructive microsurgery. Plast Reconstr Surg. 2008;121:88–94.
121. Jacobson AS, Eloy JA, Park E, Genden EM.Vesseldepleted neck: techniques for achieving microvascular reconstruction. Head Neck. 2008;30:201–7.
122. Roumanas ED, Freymiller EG, Chang TL, Aghaloo
T. Implant-retained prostheses for facial defects:
an up to 14-year follow-up report on the survival
rates of implants at UCLA. Int J Prosthodont.
2002;15:325–32.
Part III
Post-operative Considerations
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