University of Groningen

The significance of preoperative vascular mapping of donor- and acceptor vessels in free flapsurgeryKlein, Steven

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Chapter 3

Donor site necrosis following fibula free flap transplantation

Klein S

Hage JJ

Woerdeman LAE

Microsurgery 2005; 25: 538-542

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Summary

The free fibula flap is the microsurgeon’s workhorse for the reconstruction of osseous or

osteocutaneous defects. Donor-site morbidity of this flap is reported to occur infrequently, and is

generally considered minor and transient. We present the case histories of three patients with necrosis

at the fibula flap donor site to stress the risks and explain the possible mechanisms of such severe

complications. The small risk of debilitating donor-site necrosis should be considered and discussed

preoperatively with the patient.

Introduction

The fibula free flap has become the microsurgeon’s workhorse for the reconstruction of osseus or

osteocutaneous defects of the head and neck region,(1-3) the extremities,(3-5) and the trunk.(3,6) Flap

survival and receptor site function after fibula flap transplantation have been evaluated extensively, but

donor-site morbidity has been assessed less often. Donor-site morbidity includes wound healing

disturbance and cellulitis,(1-3) transient peroneal sensory loss or cold intolerance,(1-4,7,8) motor

weakness of lower leg muscles,(1,4-9) pain or occasional cramp,(1-4,7-9) impingement of the peroneal

muscle,(10) edema after prolonged standing,(2-4,8) and ugly scarring.(4) Even though valgus deformity,

instability, or stiffness of the ankle,(1,2,4,7-9,11) and walking restriction or gait disturbances,(2,3,5,6)

can be considered more serious donor-site complications, most of the complications mentioned above

are generally rated as acceptable by patients.(1,2,4,6,8,9)

Major donor-site complications with extensive wound breakdown or necrosis are generally considered to

occur infrequently after fibula free-flap transfer. To date, only five cases of such debilitating

complications due to necrosis have been reported to lead to deep necrotectomy. Among these five were

two cases of acute compartment syndrome,(3,12) two cases of late necrosis,(13) and one case of

necrotizing infection.(4) To stress that such donor-site necrosis can lead to severe postoperative

disability, we present three more patients who suffered from extensive necrosis of the lower leg, and we

discuss how to prevent these complications.

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Case reports

Patient 1

A 36-year-old woman underwent commando resection and supraomohyoidal lymphadenectomy for

T4N0M0 squamous-cell carcinoma of the floor of the mouth and left hemimandible. Her medical history

included systemic lupus erythematosis, tobacco abuse, and a mild myocardial infarct sustained 2

months prior to surgery. Because preoperative angiography showed no acquired or congenital

anomalies of the crural arteries, the defect was reconstructed using a fibula free flap, including a

significant part of the lateral hemisoleus muscle and a skin segment of 6 x 14 cm (Fig.1). Per our

routine, no tourniquet was used during surgery. The donor defect was closed primarily over a suction

drain after loose approximation of the muscles of the lateral compartment. No attempt was made to

approximate the lateral fascia. The lower leg and foot were splinted on a dorsal cast to prevent pes

equinus, and the patient was kept on subcutaneous heparin prophylaxis. No pressure or tensor

bandage was applied to the leg, but the patient was required to keep the leg elevated until mobilization,

one week postoperatively.

On the first postoperative day, however, the patient complained of pain in the donor leg and sensory

loss of the dorsum of the foot. On physical examination, there was functional loss of the extensor

digitorum muscle, decreased capillary refill of the foot, and lack of a Dopptone signal over the dorsal

tibial artery. These symptoms being indicative of compartment syndrome, the cast and skin sutures

were removed to reduce tension in the calf.(14,15) Angiography subsequently showed arterial filling of

both tibial arteries (Fig.2). Still, necrosis of the extensor digitorum muscle and parts of both peroneal

and long flexor hallucis muscles occurred, and repeated necrotectomy had to be performed surgically,

on postoperative days 11 and 22. After this, the crural wound healed except for its most distal part

(Fig.3). Six months after surgery, part of the distal fibula remnant still protruded from the wound, and X-

ray examination could not exclude osteomyelitis. Consequently, this part was resected, and the

remaining bone was covered during a fourth and final surgical procedure. When last seen at 44 months

of follow-up, the patient was free of recurrence, and the neomandible was functional. However, her gait

and walking distance were severely impaired.

Figure 1. Design of fibula free flap used on patient 1. Flap included significant part of lateral hemisoleus

muscle, and skin segment measuring 6 x 14 cm.

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Figure 2. Postoperative angiography of patient 1 showed arterial filling of both tibial arteries.

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Figure 3. Six months after fibula free-flap transplantation in patient 1, distal part of crural wound had not

closed, and protruding part of distal fibula remnant was resected.

Patient 2

A 74-year-old woman with a history of alcohol and tobacco abuse underwent commando resection and

modified radical lymphadenectomy for a T3N0M0 squamous-cell carcinoma of the floor of the mouth

extending to the left hemimandible. As the preoperative angiography showed no vascular anomalies,

the defect was reconstructed using an osteocutaneous free fibula flap with a skin paddle of 5 x 12 cm.

As no tourniquet was used intraoperatively, it could be confirmed that the manipulated muscles

remained well-vascularized throughout the entire procedure. Following approximation of the donor-site

muscles, the lower leg skin defect was covered with a split-thickness skin graft to avoid undue pressure,

and the lower leg and foot were splinted to prevent pes equinus. Again, no tensor bandage was applied,

and the patient was required to keep the leg elevated until mobilization, 1 week postoperatively.

The postoperative course was uneventful up to day 15, when edema occurred in the donor leg. Even

though wound cultures remained negative for necrotizing species, subsequent necrosis of the skin graft

and surrounding skin and subcutaneous tissue necessitated necrotectomies on postoperative days 23

and 37 (Fig.4). The resulting skin defect measured 10 x 25 cm, and skin grafts were applied

secondarily. Using a vacuum-assisted closure system, the wound completely healed by 10 weeks after

primary surgery. At 24 months of follow-up, the patient was free of recurrence, and her neomandible

functioned adequately. No remaining functional loss of the donor leg was observed.

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Figure 4. In patient 2, skin defect resulting from initial surgery, postoperative ‘‘pseudo’’-compartment

syndrome, and subsequent necrotectomy measured 10 x 25 cm.

Patient 3

A 56-year-old diabetic man underwent segmental mandibulectomy for residual ameloblastoma, after

local resections had twice been attempted elsewhere. Because the preoperative angiography showed

no atherosclerosis or vascular anomalies, the left hemimandible and gingiva defect was reconstructed

with a fibula osteocutaneous free flap. The skin paddle measured 6 x 11 cm, and was raised on one

mid-lower leg muscular perforator, as no adequate septocutanous vessels were found. This perforator

had a long intramuscular course and a peroneal origin near the crural trifurcation, and several muscular

branches originating from the peroneal artery had to be clipped to allow for its dissection. Again, no

tourniquet was used, allowing for proper hemostasis and assessment of the muscles that were

manipulated during flap dissection. Following microsurgical flap transfer, the lateral lower leg muscles

were loosely approximated, and no attempt was made to close the fascia. The skin was partly closed

primarily, and partly by use of a skin graft. A splint was applied to prevent pes equinus, and the patient

was kept in bed and on heparin prophylaxis for 1 week. No tensor bandage was applied.

The postoperative course was uneventful until the patient became febrile and complained of pain in the

donor leg on postoperative day 11. Wound culture was positive for beta-hemolytic Streptococcus, and

antibiotic therapy was initiated. At surgical exploration, the long peroneal muscle was found to have

necrosed. Following necrotectomy, it took 10 weeks of extensive conservative treatment, including

application of a vacuum-assisted closure system, for the wound to heal. When last seen at 24 months of

follow-up, the patient was free of recurrence of osteoblastoma, and his neomandible was functional, but

exorotation and plantar flexion of the foot were compromised.

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Discussion

Fibula flap donor-site morbidity and its consequences for daily life function are generally considered to

be rare and minor. Still, we observed severe donor-site necrosis in 3 of 74 patients in whom a fibula flap

transplantation was performed in the Netherlands Cancer Institute from January 1985 until December

2003. The mechanism of necrosis may differ. Our first patient represented an obvious case of acute

compartment syndrome, whereas a delayed ‘‘pseudo’’-compartment syndrome and a necrotizing

infection were the probable causes in our second and third patient, respectively.

Compartment syndrome is allegedly a rare consequence of free fibula flaps, and has been reported only

twice to date.(3,12) This syndrome occurs when intra-compartment pressure builds up in cases where

the fascia surrounding the compartment is intact. Obviously, this is no longer true in cases where the

lateral fascia is not closed after fibula flap transplantation. In these cases, closure of the skin under

excessive tension may be a cause of compartment syndrome, and there- fore it has been advised to

restrict primary closure of the donor site to skin paddles of maximal 6-cm width.(13,16) Alternatively,

compartment pressure may build up as a result of edema, even in cases where skin closure was

performed without undue tension.(13) In both instances, the skin acts analogous to the fascia, and

complete release of the wound may be expected to alleviate the ‘‘skin compartment syndrome.’’

In our first patient, the width of the skin paddle was restricted to the 6-cm maximum. Moreover, part of

the lateral hemisoleus muscle was harvested along with the flap, and this may be expected to reduce

the circumference of the leg and hence the closure tension. Even after adequate response to symptoms

presenting on the first postoperative day,(14,15,17) necrosis of some muscles of the anterior, lateral,

and deep compartments occurred, and hence we feel that avoidance of primary skin closure might have

prevented the compartment syndrome.(12) More careful patient selection might not have prevented the

occurrence of compartment syndrome in this patient. Such occurrence has been associated with age

under 35 years, male sex, diabetes mellitus, obesity, hypertension, traumatic rather than surgical injury,

bleeding disorders or the intake of anticoagulant drugs, low preoperative ankle-arm index, extended

duration of surgery or surgery in the lithotomy position, intraoperative hypothermia or hypotension, and

the postoperative use of regional nerve blockades.(18-22) Furthermore, patients suffering from

peripheral vascular disease were reported to run a higher risk of compartment syndrome when a

tourniquet was used during surgery.(18,20) Except for the duration of surgery, none of these

predisposing factors applied to this patient.

As for our second patient, we feel that the tension that developed in the lower leg after some delay was

too high, notwithstanding the use of a skin graft. The physical mechanism underlying the development

of the delayed necrosis seems to have been a vicious cycle of excessive tension caused by edema

leading to tissue damage and increased capillary permeability.(13) The resulting intercellular pressure

and soft-tissue edema led to more tissue damage and an increase of venous, lymphatic, and arterial

vessel compression, thus perpetuating the cycle. This cycle of gradually increasing ischemia has been

termed ‘‘pseudo’’-compartment syndrome, and may explain why the symptoms in this patient only

presented after 15 days.(13)

Paradoxically, fibulectomy used to be the treatment modality for lower leg compartment

syndrome.(14,17) Still, fibulectomy may not prevent occurrence of the complication. Rather than closing

the wound primarily, we currently apply a skin graft, irrespective of the width of the skin paddle included

in the flap. Often, this graft can safely be resected after the period of edema has passed. Still, a delayed

29

‘‘pseudo’’-compartment syndrome may develop, even in cases where a skin graft was used.(13) To

minimize the damage secondary to (‘‘pseudo’’-) compartment syndrome, we advise the surgeon to be

postoperatively alert to clinical symptoms such as pain that seems disproportionate to the clinical

situation, pain on passive stretch of the muscles, or decreased sensibility in the distribution of the

nerves running through the corresponding compartment.

The necrosis at the donor site in our third patient was likely caused by the combined occurrence of beta-

hemolytic Streptococcus and long-term muscle ischemia as a result of the obligatory clipping of multiple

vascular branches to the long peroneal muscle. Additional pre- disposing risk factors for such local

ischemia include atherosclerosis or vasculitis, endothelial damage, abnormal blood constituents due to

coagulation, fibrinolytic changes or hyperviscosity, and decreased blood flow as a result of

immobilization or vascular compression.(23) The risk factors for atherosclerosis are age over 65 years,

diabetes mellitus, obesity, tobacco abuse, hypertension, hypercholesterolemia, and a sedentary

lifestyle.(24) Our patient was a smoker, suffered from diabetes mellitus, and was expected to be

immobile for some days after surgery, but the need for extensive devascularization of the peroneal

muscle could not have been foreseen preoperatively. As was true for our other two patients, more

careful patient selection might not have prevented the donor-site necrosis in this patient.

We conclude that donor-site morbidity after fibula transfer is generally minor, but there is a small risk of

donor-site necrosis as a result of acute compartment syndrome, delayed ‘‘pseudo’’-compartment

syndrome, or necrotizing infection. This risk and its predisposing factors should be preoperatively

discussed with the patient, as donor-site necrosis may result in debilitating long-term morbidity.

Perioperatively, the risk of such necrosis should be minimized by closure of the wound with a skin graft,

and postoperatively, necrosis should be considered upon presentation of any disproportional local

symptom.

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