Delayed microsurgical reconstruction of the extremities for complex soft-tissue injuries

DELAYED MICROSURGICAL RECONSTRUCTION OF THEEXTREMITIES FOR COMPLEX SOFT-TISSUE INJURIES

MICHELE RICCIO, M.D.,* PIER PAOLO PANGRAZI, M.D., ANDREA CAMPODONICO, M.D., and ALDO BERTANI, M.D.

The treatment of severe wounds of the extremities, characterized by large posttraumatic tissue loss, represents a clinical problem difficultto resolve, especially when the lesion is surrounded by large areas of ischemic distrophic tissue which progressively aggravate andextend the initial lesion, with frequent exposure of bone and joint structures making the amputation of the limb an inevitable outcome.The authors present their experience based on combined treatments by medical support methods such as hyperbaric oxygen (HBO) andvacuum-assisted closure therapy (VAC) and microsurgical reconstruction of the limbs, within a precise therapeutic protocol. The use ofthis protocol in appropriate times and ways allowed us to successfully treat severe posttraumatic sequelae of the limbs, avoiding thedelayed healing typical of these pathologies, both on the donor site of the flap and on the repaired area, and avoiding unsuitablemicrosurgical reconstruction of limbs, allowing satisfactory morpho-functional restoration and a reduction of the hospitalization period.ª 2005 Wiley-Liss, Inc. Microsurgery 25:272�283, 2005.

In the treatment of severe lesions of the limbs due tocrush injuries, microsurgical repair methods can besupported by therapies that lead to a quick and com-plete resolution of the clinical situation.

There is no doubt that free tissue transfer by the useof microsurgical techniques is now routine for the sal-vage of traumatized extremities.1�3

As a matter of fact, this method represents the besttreatment in acute and severe trauma of the limbs wherelarge exposures of vascular and nervous structures andbone fractures are involved.

In these cases, but with wounds uncontaminated byexogenous material, the indication exists for large de-bridment of devitalized areas around the lesion andcoverage by a free flap within 72 h from the trauma.4,5

On the other hand, in severe traumas of the limbscontaminated by mineral oils, ground and vegetable fi-bers, ormaterial from the asphalt sometimes coming fromroad traumas, it is compulsory to clean the site of traumabefore the microsurgical coverage, to avoid the risk ofserious infection or septic pseudoartrosis that couldundermine the success of the reconstruction procedure.

In these cases, it seems opportune to differ thereconstructive time, employing all the medical supportat the disposal of the surgeon (hyperbaric oxygen(HBO), vacuum-assisted closure therapy (VAC), andspecific antibiotic therapies) and further repeated de-bridments to clean the site of the lesion.5�8

In the same way, the introduction of microsurgerytechniques allows us to resolve a great number ofposttraumatic chronic ulcers cases of the limbs thanksto the transplant of well-vascularized tissue on the siteof a lesion, after the excision ‘‘en bloc,’’ with the ulcer,of all dystrophic tissue around it which prevents heal-ing.9

However, it sometimes happens that the ‘‘zone ofinjury’’ caused by the inflammatory response of the softtissue around the ulcer is not so evident, making theradical treatment difficult that should include debride-ment of all devitalized, dystrophic, and contaminatedtissue around the ulcer.5

Hence the radical exeresis could involve demolitionof a too wide area, which is difficult to repair, especiallyin the limbs, even with microsurgery procedures, be-cause the real extension of the zone of injury is largerthan the visible zone.

As a matter of fact, whenever the transfer of a freeflap does not allow us to entirely replace the dystrophictissue around the ulcer, either because of its size or be-cause the presence of areas of devitalized tissue aroundand below the ulcer makes it difficult to mark theboundaries macroscopically, some inevitable sequelaeare foreseable, e.g., local infections, wound diastases,fistolae, and at a later stage, homologous ulcerative le-sions in the anatomical areas adjacent to those whichhave been repaired, which usually require multiple sur-gical procedures.10

In our experience, we have observed that in severeand wide lesions of the limbs, microsurgery procedurescan be successfully combined, after debridement, withHBO, VAC, and selective antibiotic therapies, whoseeffect is to limit the extension of the area to be repaired,improve the trophism of the chronically inflamed tissuearound the ulcer, and create the conditions most suitablefor the implant of free flaps.

Hand Surgery and Microsurgery Unit, Department of Plastic and Recon-structive Surgery, School of Medicine, University of Ancona, AnconaTeaching Hospital, Torrette di Ancona, Italy

*Correspondence to: Michele Riccio, M.D., Clinica di Chirurgia Plastica eRicostruttiva, Universita Politecnica delle Marche, Azienda Ospedaliera‘‘Ospedali Riuniti Umberto I—Lancisi—Salesi,’’ Via Conca 71, 60020 Torrettedi Ancona, Italy. E-mail: [email protected]

Received 28 February 2005; Accepted 8 March 2005

Published online 2 June 2005 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/micr.20132

ª 2005 Wiley-Liss, Inc.

MATERIALS AND METHODS

Patient Database

From 1999�2003, 8 patients were treated, sufferingfrom severe large lesions of the skin and soft tissue of thelimbs, with exposure of bone and joint structures inconsequence of serious crush injuries (Table 1).

Whatever the origin, the treatment consisted of acombination, at different prefixed stages, of debride-ment surgical procedures, medical support methods, anddefinitive surgery by microsurgical free-tissue transfer.One case required an additional free-flap transfer for thetreatment of a dystrophic ulcer of the forefoot, whichoccurred on the previous muscular free flap at thegrafted surface (Table 1).

The average age of patients (6 men and 2 women)was 23.25 years, ranging from 8�58.

The follow-up period ranging from 6�36 months.Patients were selected for the combined medical

support methods and microsurgery protocol accordingto the following criteria:

1. Severe crush injury of the limbs with large tissueloss;

2. Massive necrosis areas 2�3 days after injury;3. Deep posttraumatic ulcers with exposures of joint,

bone, and tendon structures;4. Wide and deep wounds, contamined by exogeneous

material, with severe bacterial infections;5. Large amounts of dystrophic tissue around the

ulcer, tending to become necrotic and ulcerous;6. No chance of spontaneous repairing;7. Repeated unsuccessful attempts to repair the ulcer

with traditional surgical procedures; and8. The possibility to maintain or recover ambulation

with the repair treatment.

The group included 8 patients (Table 1) who pre-sented ulcers due to crush injury, in 7 cases of the lowerextremities, and in 1 case of the upper limb, with tissueloss and exposure of bones and tendons. One patientshowed posttraumatic gas gangrene. All were consideredfor a three-phase protocol: debridement, medical sup-port methods, and microsurgical procedures.

MEDICAL SUPPORT METHODS

HBO Treatment

In all cases in which HBO was chosen, a minimumof 10 sessions at 2.5 Absolute Tension Atmosphere(ATA) was necessary. In each of these, once thetreatment pressure level was reached with air, 100%oxygen was administered through a hermetic mask for30 and 20 min with an interval of 5 min air-breathing,

then returning to normal atmospheric pressure at aspeed of 1 m per minute oxygen breathing.11

Only in the case of gas gangrene, after emergencydecompressing fasciotomies, was an ‘‘intensive treat-ment’’ protocol chosen, i.e., the one applied in 1961 byBrummelkamp et al.,12 based on a chamber pressure of 3ATA and 100% oxygen ventilation for four periods, fora total of 90 min (20 min + 20 min + 20 min + 15min), separated by corresponding 5-min periods of air-breathing in order to decrease the toxic effect of oxygen.This treatment was repeated three times in the first 24 h,with the first two sessions separated by a 2-h interval.This treatment was repeated for the following 24 h every12 h, and then every 24 h for a total of 7 sessions in 4days.

In this protocol, HBO treatment was always pre-ceded by radical debridement of the ulcer and the dys-trophic tissue around it, and came before the definitiverepair procedure, usually consisting of the transplant ofa free flap.

Vacuum-Assisted Closure Therapy

VAC is designed to promote the formation ofgranulation tissue for faster healing in the wound bedsof patients with acute and chronic wounds, and we haveused this approach in both devitalized and infectedtissue.

The VAC device consists of a noncollapsible, open-cell, polyurethane sponge with embedded vacuum tub-ing, a vacuum pump, and transparent adhesive dressing.The wound management technique exposes the woundbed to negative pressure by way of a closed system.

Theoretically, the method acts by removal of excesstissue fluid from the extravascular space, which lowerscapillary afterload and thereby promotes the microcir-culation and proliferation of exuberant granulation tis-sue during the early stages of inflammation.13,14

Microsurgical Procedures

In all patients in whom the definitive repair of anulcer was obtained through microsurgical procedures(Table 1), the transfer of the free flap was preceded by aroutine vascular scan of the limbs involved in thepathology.

Limb perfusion was always assessed clinically, whilethe site of the potential microvascular anastomosisneeded a meticulous evaluation with Doppler mapping,which can give reliable information without the need forroutine angiography of the recipient site.15

In particular, the ‘‘directional Doppler-flow’’ allowsus to check the quality of the blood flow, while echo-Doppler visualizes the atherosclerotic areas responsiblefor hemodynamic problems.

Microsurgical Reconstruction of Limbs 273

Table

1Seve

reTraumatic

Ulcers

TreatedWith

MedicalSupportMethods*

No.Patie

nt

Age

Lesion

Priorprocedures

Freefla

pPost

procedures

Complicatio

ns

Treatm

ent

Outcome

1M.D.

15

Traumatic

deglovingof

leftfootforcrush

injury

Forefootamputatio

n+

debridement

offootdorsum

andso

le+12HBO

sessions

LeftLDF+sk

ingrafts

onso

le+

skin

graftsondorsum

None

Six

monthslater,

decubitu

sulcer

forefootwith

exp

osu

reoffirst

andse

cond

metatarsal

bone

Debridement+

12HBO

sessions

+leftRFCF

Successful,follow-up

at21months

2O.M

.18

Traumatic

ulcerof

leganddorsum

of

leftfootforcrush

injury,

complicatedby

gasgangrene

Debridement+7HBO

emergencyse

ssions

Rightparasc

apolarfla

pNone

None

None


at24months

3D.G

.28

Lateralmalleolar

posttraumatic

ulcerwith

right

astragalo-calcaneal

osteomye

litis

secondary

toposttraumatic

osteosynthesis

Superficial

debridement+

targeted

antib

iotic

therapy

+12HBO

sessions

Radicaldebridementof

bone+leftRFCF

None

None

None


at36months

4N.R.

58

Posttraumatic

ulcerof

rightlegse

condary

tocrush

injury

Debridementofskin

andbone+12HBO

sessions

LDM-C

F+autologous

graft

offib

ula

protib

ia

None

None

None


at36months

5N.M

.19

Posttraumatic

ulcerof

leftlegfollowinga

fracture,with

tibio-peroneal

exp

osu

re

Skinandbone

debridement

+12HBO

sessions

Serratusanterior+

skin

grafts

None

None

None


at36months

6G.M

.30

Posttraumatic

ulcerof

rightheelfollowing

crush

injury

Skindebridement+

12HBO

sessions

LDM-C

F+sk

ingrafts

None

None

None


at12months

7G.I.

10

Posttraumatic

ulcerof

dorsum

ofrightfootfor

crush

injury

Skinandbone-

debridement

+14HBO

sessions

Serratusanterior

+sk

ingrafts

Flapdegraissa

ge

after2ye

ars

None

None


at26months

8C.D.

8Traumatic

ulcerbyavu

lsion

ofleftarm

,with

median

nerveandelbowjointlesion

Multiple

skin

debridement+

25HBO

sessions

ALTPF+nervegraft

+jointrepair+

engineeredtissu

ebyautologus

fibroblasts

andke

ratin

ocytescultu

re

Release

ofsc

ar

retractio

nofelbow

and

wrist

+sk

ingrafts

None

None


at6months

*LDF,latissirnusdorsifla

p;RFCF,radialfasc

io-cutaneousfla

p;HBO,hyp

erbaricoxy

gentherapy;

LDM-C

F,latissimusdorsiMyo

cutaneousfla

p;ALTPF,antero-lateraltig

htperforatorfla

p.

274 Riccio et al.

Such an accurate study allows for the choice of the bestrecipient site for anastomoses, drastically reducing therisk of failure.

In only 2 cases was it necessary to complete the studyof the vascular anatomy of the limbs with angiography.

In our opinion, an arteriogram should be consideredif the zone of injury is wide and in the region of potentialanastomoses.5

The timing of microsurgical tissue transplantationwas delayed 10�15 days, in accordance with our‘‘combined protocol therapy.’’

Nine free flaps were transplanted for the treatmentof ulcers, of which 4 were fasciocutaneous flaps, 2 weremyocutaneous flaps, and 3 were muscular flaps.

We used:2 radial fasciocutaneous flaps;1 latissimus dorsi muscular flap, and 2 latissimusdorsi myocutaneous flaps;1 parascapolar fasciocutaneous flap;2 serratus anterior muscular flaps; and1 antero-lateral tight perforator flap.

Regarding the reconstruction of lower extremities,anastomoses were mainly end-to-side on the posteriortibial artery in order to prevent angiospasm, typical ofthe lower extremities, and to save an artery which isessential to foot vascularization, especially in patientssuffering from chronic diseases such as diabetes andconnective inflammation.

As a matter of fact, in these patients, when the initialphase of microangiopathy was followed by macroangi-opathy due to atherosclerosis, sacrificing one of the twomain arteries reduced the possibility of efficient shunting.

In 8 cases, the flap was transplanted with an end-to-side anastomosis on the posterior tibial artery.

In only one case, already treated for the repair ofa crush injury of the foot by the transplant of a la-tissimus dorsi muscolar free flap, with end-to-sideanastomosis on the posterior tibial artery, was thetransplant of a second free flap (RFCF) effected, foranatomical reasons, by end-to-end anastomosis withthe anterior tibial artery, in order to repair a furtherdystrophic ulcer of the sole on the grafted surface ofthe muscular flap.

In the case of an avulsion injury of the upper limb,there was a stop of the brachial artery at the distal thirdof the humerus, the forearm and the hand were vascu-larized by collateral circulation.

In this case, arterial anastomoses was performedend-to-end between the brachial artery and the pedicleartery of the Antero-Lateral Tight Perforator Flap(ALTPF), and venous anastomoses was performed be-tween the comitantes veins.

CASE REPORTS

Case 1 (Table 1), M.D., age 15, came under obser-vation following a left-foot crush injury, 14 days afterthe trauma had been treated elsewhere only by meta-tarsal fracture reduction.

The plantar and dorsal skin was completely necrotic(Figs. 1, 2).

Immediate debridement of the necrotic tissueconsisted of the ‘‘en bloc’’ exeresis of the dorsal footskin, muscles, and tendon tissue of the plantar area, aswell as the amputation of the toes, distal to the meta-tarsal-phalanx joints. Afterwards, he was treated withHBO (12 sessions) according to the already-describedprotocol (Fig. 3).

On day 16, resurfacing of the foot was carried out bythe transfer of a left latissimus dorsi flap for the sole,while the dorsum was covered by a medium-thicknessskin grafts (Figs. 4, 5).

After 6 months, despite good viability of the flap asshown by angiography, the patient presented an ulcer ofthe forefoot due to decubitus of the metatarsal bonestumps of the first and second toes, made more seriousby a dystrophic area around the ulcer (Figs. 6, 7).

For repair of the ulcer, a therapeutic protocol wasfollowed, again consisting of HBO treatment (12 ses-sions) following debridement of the dystrophic area.

Afterwards, an integumental covering was obtainedthrough the transplant of a second free flap, i.e., a fas-ciocutaneous radial flap.

Twenty-one months’ follow-up showed no sign oftissue dystrophy, and the covering tissue appears trophicand well-vascularized. The patient’s ambulation is sat-isfactory (Figs. 8, 9).

Case 8 (Table 1), C.D., 8, was treated for a severeavulsion and crush injury of the left arm and forearmfollowing a car accident.

This lesion caused also a fracture and complete dis-location of the elbow with a rupture of the biceps ten-don, interruption of the brachial artery, and loss of themedian nerve for 10 cm (Figs. 10, 11).

Angiography showed the interruption of the brachialartery, but the clinical evaluation and Doppler asses-ment showed a good radial pulse at the wrist and anoptimal peripheral flow (Fig. 11).

Hence we did not repair the continuity of the bra-chial artery toward the artery of the forearm, for thesake of the growth of an effective collateral circulationfor the forearm and the hand.

After the immediate first debridement, the patientunderwent 25 HBO sessions and further debridementsfor extreme contamination by ground and vegetablefibers and for a progressive enlargement of the necroticarea (Fig. 12).


In the same operative section, repair of the elbowfracture was performed as well as the arthroplasty of theelbow joint, using a graft of the fascia lata and thereconstruction of the median nerve, using a double graft

of the sural nerve (Fig. 13). In the same operative sec-tion, the covering was undertaken through the trans-plant of the ALTPF after 27 days, when no signs ofinfection were found (Fig. 14).

Figure 3. Case 1 (M.D.). Preoperative aspect of foot after 12 HBO

treatments and several debridements.

Figure 4. Case 1 (M.D.). Harvesting latissimus dorsi muscular flap.

Figures 1, 2. Case 1 (M.D.). Crush injury of left foot. Both sole and dorsum were involved.

276 Riccio et al.

The resurfacing of the forearm was completed withengineered tissue by a culture of autologus fibroblastsand keratinocytes, in order to limit the extension of scardebit (Fig. 15).16

Six months’ follow-up showed no sign of tissuedystrophy, and the covering tissue appeared trophic andwell-vascularized.

The functional ability of the upper limb is improving(Figs. 16�19). The patient is awaiting the last operativeprocedure to gain active flexion of the elbow by thetransposition of a functional latissimus dorsi myocuta-neous island flap.17,18

RESULTS

All patients treated with medical support methodsand microsurgery tolerated the therapy well, withoutdeveloping problems in any of its phases.

In particular, no form of immediate intolerance toHBO was registered, nor did systemic sequelae appearduring the follow-up period.

Only in two cases treated by HBO therapy did thepresence of the sequelae of otitis media in one andchronic sinusitis in another cause difficult pressurecompensation between the environment and the mediumear.

However, this did not reduce the effectiveness ofHBO treatment in injuries, nor has it had any conse-quence for the patients.

The combined protocol (medical support methodsand microsurgery) allowed the complete and quick res-olution of the clinical problem in the case of large lesionsdifficult to treat by traditional nonmicrosurgical proce-dures, creating the anatomic conditions most suitablefor a flap transplant and therefore reducing the inci-dence of sequelae.

HBO, accelerating the healing process, makes itpossible to transplant flaps on recipient well-vascular-ized trophic beds, and favors the taking of free skingrafts from donor sites.

In our experience, any time we used HBO treatmentin accordance with the combined protocol afterdebridement and before definitive wound managementby free-tissue transfer, no complication occurred at therecipient site, and a considerable reduction of chronicphlogosis around the lesion was observed. A well-vas-cularized tissue bed received the free flap.

On the other hand, any time we immediately repairedsevere and contaminated lesions by microsurgery flaptransplant after debridment, without applying the com-bined protocol, in spite of a large exeresis before thetransplant, several sequelae were observed both at therecipient site and at the donor site, delaying the healing ofthe wound, or making amputation of the limb inevitable.

In particular, we observed, in accordance with theliterature, a high incidence of postoperative infections,fistulae, and surronding tissue necrosis, with delayedhealing (Table 2).

DISCUSSION

The treatment of mangled extremities still presents areconstruction challenge difficult to resolve and some-times an emotional problem, whose sequelae demanded,in a recent past, the frequent amputation of the limbwhen an insufficient blood inflow determined the pro-gressive deterioration of the ulcers.10

The massive extremity injuries following crush high-energy traumas, characterized by massive necrosis ofwide soft-tissue areas and infections with large expo-sures of bone fractures and joint structures, were themain indications for limb amputation.19

There is no doubt that in all these cases, microsur-gery procedures allowing the transfer of viable autolo-gous tissue and, where necessary, reestablishingcontinuity between the main vessels, enabled the en blocreconstruction of the morpho-functional unit withoutsize limits, and an aesthetic and functional recovery ofthe limb,9,20 sometimes allowing surgeons to salvageextremities in patients who would formerly have re-quired amputation.1�3

Also, in less wide lesions, microsurgery proceduresare preferred to traditional ones because of the smallernumber of sequelae and deficits at a local level.

The most important factors influencing the micro-surgical reconstruction of the limbs are:

the selection of a free-flap; andthe timing for microsurgical reconstruction of theextremities.

Figure 5. Case 1 (M.D.). Outcome of foot reconstruction with

latissimus dorsi muscular free flap covered by split thickness skin

grafts.


Primarly, the choice of flap depends on the recipientsite requirements or the type of tissue deficency (isolateor composite replacement) and its volume.

The length of vascular pedicle should allow anasto-moses in a ‘‘safe zone’’ far from the ‘‘zone of injury,’’where the inflammatory response of the soft tissue

Figures 8, 9. Case 1 (M.D.). After 12 HBO tratments and radical debridement of ulcers, forefoot was resurfaced by transplant of radial

fasciocutaneous free flap. Result after 21 months.

Figures 6, 7. Case 1 (M.D.). After 6 months, despite good viability of flap as shown by angiography, some ulcers of forefoot occurred.

278 Riccio et al.

around the wound increases the vascular friability andperivascular scar tissue, causing a higher rate ofmicrovascular thromboses, especially localized in theveins.21

The timing for the microsurgical reconstruction ofthe limbs is a most important prognostic factor thatemphasizes the importance of radical debridment andearly tissue coverage within the first 72 h in the treat-ment of high-energy traumas.4

But frequently, the massive soft-tissue necrosis andcontaminated surrounding tissue require several de-bridements to obtain a good prognosis in terms of de-creased risk of infection and flap survival.22

In these severe traumatic ulcers of the limbs, the keyfactor considered in the timing of microsurgical recon-struction is the ‘‘risk of infection’’ in the presence ofexposed ‘‘vital structures.’’

Hence on the basis of the ideal ‘‘reconstructive lad-der,’’ the surgeon should decide to perform the ‘‘primarycoverage’’ by a free flap only when the bacterial status ofthe wound allows microsurgical reconstruction withoutrisk of infection, within 7�15 days after the initialdebridement, using that period to prepare the recipientsite by medical support such as HBO or VAC therapy.5

The best repair procedure for infected and ischemicwounds,23,24 with chronic osteomyelitis is the micro-surgical transfer of muscular flaps because providecoverage for the debrided bone, obliterate dead space, aswell as improves vascularity and enhance leucocytefunction,24-26 but frequently muscle flap closure for limbdefect has a significant postoperative local sequelae rate,such as severe infection that may subsequently result inloss of flap tissue or the difficult taking of skin grafts onthe transplanted muscle.

The consequence of all this is often an unsatis-factory recovery of limb function. From this point ofview, the medical support method of tretmentconsiderably improved the prognosis in the abovecases.

The effect of HBO therapy seems to be particularlydramatic in reducing the physiopathologic problemsresponsible for cutaneous dystrophic diseases, whichrarely heal spontaneously.

The healing process of a wound is oxygen-depen-dent, as shown by the fact that all the wounds that donot heal are hypoxic and more prone to infections.27�29

Wound healing takes place thanks to macrofages,fibroblasts, and collagen synthesis.

Figures 10, 11. Case 8 (C.D.). Severe avulsion and crush injury of left arm and forearm with fracture and dislocation of elbow, rupture of

biceps tendon, and interruption of brachial artery.

Figure 12. Case 8 (C.D.). After debridement and surgical excision of

non viable soft tissue, patient was subjected to 25 HBO sessions.


Hypoxia slows down the synthesis and metabolismof collagen proteins through the inhibition of prolineand lysine hydroxylation.

In this condition, the collagen produced appears tobe less stable and less resistant to tension, the lack ofidroxyproline and hidroxylysine being an obstacle to theformation of intermolecular cross-links.30

Moreover, although the healing process is triggeredby hypoxia, the migration and intervention of themacrofages and fibroblasts are inhibited by pO2 valuesof less than 10 mmHg at the wound level.

In this microenvironment, the production of newangiogenesis factors by the macrofages is inhibited, inconsequence of scarce granulation tissue.31,32

This effect can be reversed, reaching optimal levels ofneoangiogenesis and growth factors by the macrofagesat a pO2 of 15�20 mmHg.33

Another serious problem is the bacterial infection ofthese ulcers, which can not only interrupt the healingprocess, but also cause a worsening of the dystrophy andwidening of the ulcer.

With HBO treatment, an adequate partial pressureof O2 on the dystrophic ulcer is reached, allowing theoxidative killing responsible for the respiratory bust bypolymorphonucleates, as well as an indirect bactericidalaction through the macrofages. All these events areoxygen-dependent.

HBO treatment at 2.8 ATA increases 10�13 fold thequantity of oxygen transported per blood unit vs. acondition of normal atmospheric pressure, because theoxygen can be physically diluted in the plasma and moreeasily carried to sites of tissue dystrophy and ischemiaaround the ulcer or to sites with blood flow obstruc-tions.11 In this physiopathological condition, HBO at2.5 ATA interrupts the strong relationship betweenischemia and edema on the dystrophic tissue around thelesion, which in turn aggravates tissue dystrophy owingto the progressive increase of intercapillary distance.34

The mechanism through which HBO works is basedon a 20% reduction of the blood flow in the limb, whichis balanced by an increase in the content of oxygen perblood unit. This means a progressive improvement ofthe microcirculation through the decrease of the pres-sure in the capillary interstices.35,36

This effect proves particularly useful in correctingthe hyperflow syndrome following the anomalousopening of arterio-venous shunts of a neuropathic ori-gin, as happens in patients with diabetes.37,38

Figure 15. Case 8 (C.D.). Postoperative result. Engineered tissue

used for skin resurfation on free flap around skin island, in order to

reduce scar debit.

Figure 13. Case 8 (C.D.). Repair of elbow joint, using graft of fascia

lata and reconstruction of median nerve with 10-cm graft of both

autologous sural nerves.

Figure 14. Case 8 (C.D.). Harvesting right ALT perforator flap,

transferred by microsurgical anastomoses on brachial artery and

venae comitantes.

280 Riccio et al.

In conclusion, themain action ofHBOmanifests itselfin the injured tissue, maintaining viability in the hypoxicphase, preventing infections and enhancing healing andthe recovery of the function through a greater diffusion ofpO2 in the stasis areas of the microcirculation.

As regards necrotic tissues, HBO, through the acti-vation of specific and nonspecific cellular cleaningmechanisms, which are more effective at tissue levels of30 mmHg of pO2, hastens the demarcation of the ne-crotic area, and prevents infection from passing toischemic tissues.

In our experience, HBO is the most widely usedmedical support method, while our experience withVAC therapy is much less extensive, only employed as acomplementary method or whenever it was not possibleto use HBO due to a patient’s problems linked tochamber compression.

We used the VAC device in only two cases of crushinjury of the lower limb. Suction (75�125 mmHg) wascontinous for the first 48 h, and then intermittent (2 minon, 5 min off).13

This initial wound-management technique exposedthe contaminated wound bed and its deep bonestructures to negative pressure by way of a closedsystem.

This system permits the removal of edema fluidfrom the extravascular space, thus eliminating anextrinsic cause of microcirculatory stasis andimproving the blood supply during this phase ofinflammation.14

After the formation of granulation tissue and whensystemic signs of infection and quantitative culturesindicated the resolution of local infection, microsurgicalprocedures for wound colsure were performed.

Figures 18, 19. Case 8 (C.D.). Active flexion and extension of fingers.

Figures 16, 17. Case 8 (C.D.). Active extension and passive flexion of elbow.


CONCLUSIONS

As far as our experience is concerned, the combi-nation of medical support methods treatment andmicrosurgery procedures represents the right solutionfor the difficult treatment of large serious wounds of theextremities due to acute injuries in which the risk ofinfection is high, either for contamination of exogenousmaterials or for the amount of nonviable tissue aroundthe limb defect.

Therefore, in these cases and in the cases which havecome under our observation, with an ulceration alreadyposttraumatic it is necessary to delay the treatment from7�14 days to permit the cleaning of the ‘‘zone of in-jury.’’

We propose a protocol in three phases:1) Radical surgical debridment, multiple if necessary;2) 10 seats of HBO or alternatively VAC therapy; and3) Microsurgical reconstruction with well

vascularized tissue.

From this point of view, the combination of medicalsupport methods before the definitive microsurgerytretament of severe and infected wounds allows us tohit the following targets:1) Reduction of the exeresis area of the dystrophic

tissue around the ulcer through HBO therapy,after the debridement, which makes the ischemicborderline tissue viable again, interrupting theprogressive development of necrosis on theboundaries of the debridement. In a clinical plan,this allows a precise macroscopic demarcation ofnonviable tissues.

2) Enhancement of wound cleansing and reparativegranulation tissue formation of the recipient bedof severe and infected wounds through HBO orVAC therapy.

3) Radical surgical excision of nonviable tissue,which are now well-demarcated, and functionaland aesthetic reintegration, no matter the size,of the tissue loss through microsurgical trans-plant of a free flap.

4) Elimination of local sequelae both on the re-cipient and the donor sites of the flap, throughadequate HBO therapy.

The use of HBO and VAC therapy, combined withdelayed microsurgical reconstruction, in a precise pro-tocol, for the treatment of severe wounds of the limbs,allows us to save injuried limbs and improve the func-tional outcome.

REFERENCES

1. Gustilo RB, Mendoza RM, Williams DN. Problems in the man-agement of type III (severe) open fractures: a new classification oftype III open fractures. J Trauma 1984;24:742�746.

2. Lange RH, Bach AW, Hansen ST Jr, Johansen KH. Open tibialfractures with associated vascular injuries: prognosis for limb sal-vage. J Trauma 1985;25(3):203�208.

3. Howe HR Jr, Poole GV Jr, Hansen KJ, Clark T, Plonk GW,Koman LA, Pennel TC. Salvage of lower extremities followingcombined orthopaedic and vascular trauma: a predictive salvageindex. Am Surg 1987;53(4):205�208.

4. Godina M. Early microsurgical reconstruction of complex traumaof the extremities. Plast Reconstr Surg 1986;78:285�292.

5. Heller LS, Levin S. Lower extremity microsurgical recostruction.Plast Reconstr Surg 2001;108:1029�1041.

6. Strauss MB. Crush injury and other acute traumatic peripheralischemias. In: Kindwall EP, editor. Hyperbaric medicine practice.Flagstaff: Best Publishing Co.; 1995. p 525�549.

7. Hoffman RD, Adams BD. The role of antibiotics in the manageentof elective and post-traumatic hand surgery. Hand Clin1998;14:657�666.

8. Barbieri RA, Freeland AE. Osteomyelitis of the hand. Hand Clin1998;14:589�603.

9. Lai CS, Lin SD, Yang CC, Chou CK, Wu SF, Chang CH. Limb-salvage of infected diabetic foot ulcers with microsurgical free-muscle transfer. Ann Plast Surg 1991;26:212�220.

10. Oishi SN, Levin LS, Pederson WC. Microsurgical management ofextremity wounds in diabetics with peripheral vascular disease.Plast Reconstr Surg 1993;92:485�492.

11. Hammarlung C. The physiologic effects of hyperbaric oxigen. In:Kindwall EP, editor. Hyperbaric medicine practice. Flagstaff: BestPublishing Co.; 1995.p 17�32.

12. Brummelkamp WH, Boerema I, Hoogendijk L. Treatment ofclostridial infections with hyperbaric oxygen drenching. A reporton 26 cases. Lancet 1963;1:235�238.

13. Deva AK, Buckland GH, Fisher E, Liew SC, Merten S,McGlynn M, Gianoutsos MP, Baldwin MA, Lendvay PG. Top-ical negative pressure in wound management. Med J Aust2000;173:128�131.

14. Webb LX. New techniques in woundmanagement: vacuum-as-sisted wound closure. J Am Acad Orthop Surg 2002;10:303�311.

15. Lutz BS, Ng SH, Cabailo R, Lin CH, Wei FC. Value of routineangiography before traumatic lower-limb recostruction withmicrovascular free tissue transplantation. J Trauma 1998;44(4):682�686.

16. Sefton MV, Woodhouse KA. Tissue engineering. J Cutan MedSurg [Suppl] 1998;3:18�23.

17. Hovnanian AP. Latissimus dorsi transplantation for loss of flexionor extension at the elbow: a preliminary report on technic. AnnSurg 1956;143:493�499.

18. Zancolli E, Mitre H. Latissimus dorsi transfer to restore elbowflexion. An appraisal of eight cases. J Bone Joint Surg [Am]1973;55:1265�1275.

19. Gregory RT, Gould RJ, Peclet M, Wagner JS, Gilbert DA,Wheeler JR, Snydor SO, Gayle RG, Schwab CW. The mangledextremity syndrome (M.E.S.): a severity grading system for mul-tisystem injury of the extremity. J Trauma 1985;25(12):1147�1150.

20. Reichle FA, Rankin KP, Tyson RR, Finestone AJ, Shuman CR.Long-term results of femoroinfrapopliteal bypass in diabetic pa-tients with severe ischemia of the lower extremity. Am J Surg1979;137(5):653�656.

21. Arnez ZM. Immediate recostruction of the lower extremity: an up-date. Clin Plast Surg 1991;18:449�457.

22. Yaremchuk MJ, Brumback RJ, Manson PN, Burgess AR, Poka A,Weiland AJ. Acute and definitive management of traumatic os-teocutaneous defects of the lower extremity. Plast Reconstr Surg1987;80(1):1�14.

282 Riccio et al.

23. Chang N, Mathes SJ. Comparison of the effect of bacterial inoc-ulation in musculocutaneous and random pattern flaps. PlastReconstr Surg 1982;70:1�10.

24. Mathes SJ, Feng LJ, Hunt TK. Coverage of the infected wound.Ann Surg 1983;198:420�429.

25. Mathes SJ, Alpert BS, Chang N. Use of the muscle flap in chronicosteomyelitis: experimental and clinical correlation. Plast ReconstrSurg 1982;69:815�829.

26. Eshima I, Mathes SJ, Paty P. Comparison of the intracellularbacterial killing activity of leukocytes in muscolocutaneous andrandom-pattern flaps. Plast Reconstr Surg 1990;86:451� 457.

27. Niinikoski J. Cellular ad nutritional interaction in healing wounds.Med Biol 1980;58:303�309.

28. Karanfilian RG. The value of laser doppler velocimetry andtranscutaneous oxygen tension determination in predicting healingin ischemic forefoot ulceration and amputations in diabetic adnon-diabetic patients. J Vasc Surg 1986;4:511�523.

29. Hunt TK. The physiology of wound healing. Ann Emerg Med1988;17:1265�1273.

30. Chvapil M, Huryc J, Erlichova E. The influence of various tensionupon proline hydroxylation and the metabolism of collagenousproteins in skin slices. Z Physiol Chem 1968;349:211� 217.

31. Hunt TK, Niinikoski J, Zderfeld BH, Silver IA. Oxygen in woundhealing enhancement: cellular effects of oxygen. In: Davis JC, Hunt

TK, editors. Hyperbaric oxygen therapy. Bethesda, MD: U.M.S.;1977. p 112.

32. Hunt TK, Pai MP. The effect of varyng ambient oxygen tension onwound metabolism ad collagen synthesis. Surg Gynecol Obstet1973;135:561�571.

33. Dvorak HF, Kaplan AP, Clark RAF. Potential function of theclotting system in wound repair. In: Clark RAF, Henson PM,editors. The molecular and cellular biology of wound repair. NewYork: Plenum Press; 1988. p 57�85.

34. Peirce EC Jr. Pathophysology, apparatus, and methodsincluding the special techniques of hypothermia and hyperbaricoxygen. In: Charles C. Thomas, editor. Extracorporeal circu-lation for open-heart surgery. Springfield, IL: 1969. p 84�88.

35. Bird AD, Telfer HB. Effect of hyperbaric oxygen on limb circu-lation. Lancet 1965;13:355�356.

36. Schraibman IG, Ledingham IM. Hyperbaric oxygen and localvasodilation in pheripheral vascular disease. Br J Surg1969;56:295�299.

37. Boulton AJ, Scarpello JHB, Ward JD. Venous oxygenation in thediabetic neuropathic foot: evidence of arteriovenous shunting?Diabetologia 1982;22:6�8.

38. Edmonds ME, Roberts VC, Watkins PJ. Blood flow in the dia-betic-neuropatic foot. Diabetologia 1982;22:9�15.


Delayed microsurgical reconstruction of the extremities for complex soft-tissue injuries

Documents

Transcript of Delayed microsurgical reconstruction of the extremities for complex soft-tissue injuries