Foot and ankle reconstruction
Foot and ankle reconstruction is possible with –
- Simple reconstruction – 90% cases
- Complex flap – 10% cases
Six angiosomes –
- Distal anterior tibial artery – anterior ankle. & The dorsalis pedis artery – the dorsum of the foot
- Calcaneal branch of PTA – medial and plantar heel
- Calcaneal branch of the peroneal artery (PA) – lateral and plantar heel
- Anterior perforating branch of PA – anterolateral ankle
- Medial plantar artery – plantar instep
- Lateral plantar artery – lateral plantar mid- and forefoot
Plantar heel has dual blood supply –> gangrene of heel means a severe vascular compromise.
Because the foot is an end organ, many arterial-arterial anastomoses provide a duplication of inflow (provides a margin of safety) –
Arterial-arterial anastomoses around the foot and ankle-
- Between anterior perforating branch of the peroneal artery and anterior tibial artery
via the lateral malleolar artery @ ankle joint
- Dorsalis pedis artery with lateral plantar artery
via direct connection @ Lisfranc joint as the DPA dip in 1st interspace
This vascular loop is critical in determining the direction of flow within the anterior or posterior tibial arteries.
- Between plantar and dorsala metatarsal arteries – via proximal and distal perforators.
(Proximal perforators are at Lisfranc joint, distal perforators are at digital web space)
- Posterior tibial artery and peroneal artery are directly connected
(Deep to the distal Achilles tendon by one to three connecting arteries)
Motor and sensory anatomy –
Sciatic nerve –> Tibial nerve &
Common peroneal nerve –> deep peroneal nerve &
Superficial peroneal nerve
Tibial nerve –
Innervates muscle of deep and superficial posterior compartment (except gastrocnemius)
Tibial nerve trifurcates deep to flexor retinaculum into –
- Calcaneal nerve
- Medial plantar nerve
- Lateral plantar nerve
All these nerve supplies all intrinsic muscles of the foot (except Extensor digitorum brevis, EDB).
Deep peroneal nerve –
Innervates extensor muscles in the Anterior compartment and then EDB.
Superficial peroneal branch –
Innervates the everting peroneal muscles of the lateral compartment
And then it pierces the fascia to become subcutaneous and provide sensibility to the lateral lower leg and dorsum of the foot.
Sensory supply –
Superficial peroneal nerve (L4, 5, and S1) –
Anterolateral skin in the upper third of the leg
It becomes subcutaneous approximately 10 to 12 cm above the lateral ankle and travels anterior to the extensor retinaculum to supply the dorsum of the foot and skin of all the toes.
Except the lateral side of the fifth toe (sural nerve) and the first web space (deep peroneal nerve).
Deep peroneal nerve (L4, LS. and S1) –
Exits the anterior compartment deep to the extensor retinaculum.
Supply and ankle and mid-foot joints, sinus tarsi, and the first web space.
The sural nerve (LS and S1) –
Provides sensibility to the posterior and lateral skin of the leg’s distal third and
The skin of the dorsolateral foot and fifth toe.
Posterior tibial nerve –
Has three branches in the tarsal tunnel –
Calcaneal branch (S1 and S2) – supplies the medial aspect of the heel pad
Lateral plantar nerve (51 and 52) supplies the lateral two thirds of the sole and the fifth and lateral fourth toes
Medial planter nerve (L4 and L5) supplies the medial one third of the sole and the first; second, third, and medial fourth toes.
Lifetime risk of ulcer in diabetic – 15%
Major cause of diabetic foot wounds – Diabetic peripheral polyneuropathy.
>80% of diabetic foot ulcers arise in the setting of neuropathy.
↑Sorbitol level intra-neurally –> principle mechanism of nerve damage.
Damaged nerve swells –> in tight anatomical compartment this can cause further damage —- “Double crush syndrome”
This can be partially reversed by nerve release surgery.
↑ Glucose –> ↑ Advanced glycosylated end products –> causes microvascular injury.
↓insulin and ↓neurotrophic factors –> ↓ed maintenance or repair of nerve.
All these factors lead to peripheral neuropathy.
Other potential causative factor of peripheral neuropathy –
- Altered fat metabolism,
- Oxidative stress, and
- Abnormal levels of vasoactive substances such as nitric oxide
Diabetes and infection –
↑ Glucose –> diminished ability of PMNs to destroy bacteria
Diminished ability to coat bacteria with antibiotics
Diabetics are especially prone to – Streptococcus and Staphylococcus
In patient with diabetic neuropathy – 80-95% of amputation are preceded by non-healing ulcer.
Arterial disease (usually located in infra-popliteal region) significantly increases risk of ulceration and amputation. Arterial disease is present in 50% cases of diabetic foot ulcers.
Although peripheral vascular disease is frequently present, peripheral neuropathy is the primary cause of foot wounds in the diabetic population.
Neuropathic Changes –
Autonomic neuropathy – loss of pseudomotor function –> anhydrosis and hyperkeratosis –> fissuring of skin –> infection.
Charcot deformities (neuroarthropathy) of the joints – 0.1% – 2.5% of diabetic population
MC joints involved – tarsometatarsal joints 30% = metatarsophalangeal joints 30% > intertarsal joints 24%> IP joints in 4%
Possible etiology –
- Neurotraumatic – joint collapse from damage that has accumulated because of insensitivity to pain.
- Osteopenia triggered by abnormalities in the RANK1/RANK-ligand/osteoprotegerin system.
Ligamentous soft-tissue injury + Synovitis + Effusion –>
Distention of the joint capsule leads to –> ligament distortion, resulting in joint instability –>
Articular cartilage erosion, with debris being trapped within the synovium.
(These changes occur due to continued use of limb due to lack of pain sensation)
Collapse of the medial longitudinal arch –> Altered biomechanics of gait –>
Heterotopic bone formation and eburnation of load-bearing surfaces
Causes overload specific parts of the foot –>
Increased focal stress –> ulceration, infection, gangrene, and limb loss.
Motor component of neuropathy –
Intrinsic foot muscle becomes atrophied and fibrotic –> leads to MTPJ extension and IPJ flexion –> excessive pressure on metatarsal head and end of toes.
Atherosclerotic disease is a common cause of non-healing foot ulcers.
Hypercholesterolemia, hypertension, and tobacco use are additional risk factors.
Other causes of ischemia in the foot –
- Thromboangiitis obliterans (Buerger disease, generally seen in young smokers),
- Thromboembolic disease.
Before planning revascularization procedure – MUST accurately diagnose which angiosome ulcer belongs to.
If the affected angiosome is directly revascularized – wound healing increases by 5O% and the risk of major amputation decreases fourfold.
|Site of ulcer||Arteriosome to be revascularized|
|Dorsum of the ankle and foot||Anterior tibial artery or dorsalis pedis
(posterior tibial artery- If connection b/w the dorsalis pedis and the lateral plantar artery is intact)
|Heel ulcers||Posterior tibial artery or
|Mid- and forefoot plantar wounds||Posterior tibial artery
(Dorsalis pedis – If connection b/w the dorsalis pedis and the lateral plantar artery is intact)
If the ideal vessel is not available – >15% chance of failure
Patient with significant peripheral vascular disease presents with gangrene – the timing of revascularization versus debridement is critical –
Stable dry gangrene without cellulitis – revascularization first.
Wet gangrene with or without cellulitis – wound debridement first followed by revascularization urgently.
Following revascularization –> wound coverage attempted only when wound shows signs of healing (appearance of new, healthy granulation tissue and neoepithelialization).
Wound healing starts to occur by 4 – 10 days following bypass and 4 weeks following endovascular procedure.
Connective Tissue Disorders-
CTD causes recalcitrant vasculitis ulcers.
e.g., systemic lupus, rheumatoid arthritis, and scleroderma
Treatment includes – steroids and immunosuppressive agents.
Wound-retarding effects of steroids are mitigated with oral vitamin A (10,000 U/d while the wound is open). Topical vitamin A is also effective.
Almost half of patients with vasculitic ulcers also have coagulopathy leading to a hypercoagulable state.
MC are – antithrombin III, Leiden factor V, protein C, protein S, and homocysteine.
Investigation should include a – coagulation profile.
Treatment of these ulcers is principally medical.
Underlying abnormalities are identified and corrected. Wound healing adjuncts are used to cause healing.
Evaluation and diagnosis of the wound –
Etiology of foot and ankle wounds is often traumatic.
MC systemic comorbidities –
- Peripheral vascular disease,
- Venous hypertension
- Connective tissue disorders
(Accompanying disease processes include infection, ischemia, neuropathy, venous hypertension, lymphatic obstruction, immunologic abnormality, hypercoagulability, vasospasm, neoplasm, self-induced wound).
- Previous treatment of the wound(s),
- Comorbid conditions
- Current medications,
- Nutritional status
- Assess the patient’s current and anticipated level of activity
If patient likely to used limb and procedure medically tolerable and technically feasible then plan – Limb salvage.
Otherwise – consider amputation.
Physical examination –
General physical examination
Examine wound – length, breadth, depth
Examine tissue involved – epithelium, dermis, subcutaneous tissue, fascia, tendon, joint capsule, and/or bone
(If bone can be felt through wound with metal probe, it is most likely to be involved.)
(Diabetic ulcer >2 cm2 –> 90% chance of underlying osteomyelitis)
Assess vascular status – PTA , DPA. If these are palpable then the blood supply is adequate.
If not palpable –> Doppler should be used.
- Triphasic flow – indicates excellent blood £low
- Biphasic sound – indicates adequate blood flow
- Monophasic sound – warrants further investigation
(Monophasic tone does not necessarily reflect inadequate blood flow.)
If the pulses are non-palpable or monophasicà noninvasive arterial Doppler studies are done.
PVRs (pulse volume recordings) at each level is obtained –
PVR amplitude <10 mmHg – indicates Ischemia.
Toe arterial pressure is <30 mm Hg – indicates ischemia
Tissue oxygen pressure levels <40 mm Hg – insufficient local blood flow to heal a wound.
Skin perfusion pressure <50 mm Hg – indicates insufficient blood flow to heal a wound.
If all these noninvasive tests suggest ischemia –> an arterial imaging study is obtained to decide – whether a vascular inflow and/or vascular outflow procedure is required.
The gold standard for revascularization- bypass surgery.
Endovascular techniques are also very effective in treating stenosed or obstructed arteries by dilation, recanalization, or atherectomy with or without stenting. These are also less invasive than bypass surgery.
Performed with a 5.07 Semmes-Weinstein filament that represents 10 g of pressure.
If patient cannot feel the filament –> protective sensation is absent
Vibration sensation tested using 128-Hz tuning fork
Pinprick sensation, or
Motor examination –
Looking at the resting position of the foot
Strength and active range of motion of the ankle, foot, and toes.
Bone architecture –
- Evaluate if the arch is stable, collapsed, or disjointed.
- Look for bony prominences.
- X-ray series of foot- AP, Lateral, Oblique.
- X-ray appearance of osteomyelitis lags behind the clinical appearance by up to 3 weeks.
- Earlier detection of osteomyelitis- best by MRI.
- MRI also differentiates between osteomyelitis and Charcot collapse.
- Bone scans are of no value in evaluation of osteomyelitis when there is an ulcer present (as increased uptake will be seen due to ulcer).
Evaluate Achilles tendon –
If the ankle cannot be dorsiflexed 10° to 15° beyond neutral –> the Achilles tendon is tight.
If the patient cannot dorsiflex his or her foot with the knee bent or straight –>
Both the gastrocnemius and soleus portions of the tendon are tight.
If the patient can dorsiflex his or her foot only when the knee is bent –>
Then the gastrocnemius portion of the Achilles tendon is tight.
Preparing the Wound for Reconstruction –
Goal of treating any wound is to promote healing in a timely fashion.
First step – establish a clean and healthy wound base.
Acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing.
Chronic wound is a wound that is arrested in one of the wound-healing stages (usually the inflammatory stage) and cannot progress further.
Acute wound –
Wound is usually well vascularized.
Simple debridement f/b
Immediate closure or NPWT
Chronic wound (aims to convert it to acute wound)–
- Correction of medical abnormalities
- Restoration of adequate blood flow,
- Antibiotics if infection is present,
- Aggressive debridement of the wound
- Debridement includes removal of the senescent cells along the edge of the wound (3 to 4 mm of the wound edge)
If the wound responds this therapy –
- Healthy granulation appears,
- Edema decreases, and
- Neoepithelialization appears at the wound edge
Negative-pressure wound therapy (NPWT) is a useful post-debridement dressing for the uninfected, well-vascularized wound – it accelerates the formation of granulation tissue, decreases wound edema and keeps the bacterial countdown.
Measuring the wound area weekly to monitor progress – the rate of normal healing is a – 10%-15% decrease in surface area per week.
At this stage, if the wound healing is not as per expected rate – adjunct to wound healing (such as growth factors, cultured skin, and/or hyperbaric oxygen) can be used.
Must be done thoroughly.
It is mostly under-performed – leaving dead or infected tissue or bone leads to persistent infection.
Biofilm is present in over 90% of chronic wounds. It penetrates every aspect of the wound and can be found up to 4mm deep to its base (as it spreads along the perivascular plane of arterioles feeding the wound bed).
Debridement should be considered complete only when normal bleeding tissue remains.
Colors of the tissue can be used as a guide for debridement –
- Muscle – red/pink, contracting
- Fat – yellow
- Bone, tendon, fascia – white
Debridement should be done till such normal appearing tissue are reached.
Debridement can also be aided by painting the base of wound with blue dye and then removing all the painted tissue.
Sequential removal of thin layers of tissue till the normal tissue is reached – is the most effective way of debridement.
Skeletal fixation –
Stabilizing – by splinting or external fixation (monoplanar frame or Ilizarov frame).
llizarov frame provides superior immobilization, allows for bone transport, and minimizes the risk of pin track infection because of the thin wire pins.
Tissue culture – Deep uncontaminated tissue cultures pre- and postdebridement should be obtained during the initial and subsequent debridement to guide antibiotic therapy.
Effective dressings should be done following debridement.
Clean and well vascularized – a moist dressing or NPWT.
Suspected unclean wound – dressing with topical antibiotics and/or biocides
Biologic debriding agents -maggots are useful in patients too ill for anesthesia.
Maggots consume all bacteria (antibiotic resistant also VRE, MRSA), as well as biofilm.
After initial debridement to clean the tissue – its important to keep the wound clean – i.e. prevent biofilm from reestablishing itself, prevent a subsequent buildup of metalloproteases (MMPs destroy the naturally produced growth factors) à this is done by – regular scrubbing or wet-to-dry dressing.
If the wound still doesn’t heals even if bed is healthy and vascularity is good then next step is adding – local wound healing growth factors such as PDGF or cultured skin or inert dermis.
Level-one evidence has demonstrated that systemic hyperbaric oxygen can also be used to convert a non-healing wound into a healthy granulating wound.
When wound shows signs of healing (healthy granulation tissue, neoepithelialization at the skin edge) – then its appropriate to close the wound (not before).
Reconstructive techniques –
Lower Leg and Ankle Flaps-
Lower leg muscles are poor pedicled flaps as most of them are type 4 muscles (segmental minor arterial pedicles).
|Muscle of leg||Distance up to which defect can be closed|
|EHL||As distal as 2 cm from medial malleolus|
|Extensor digitorum longus
|As distal as 2 cm from medial malleolus|
|Peroneus brevis||As distal as 4 cm from medial malleolus|
|Flexor digitorum longus||As distal as 6 cm from medial malleolus|
|Soleus muscle (type 2 muscle)||anterior lower leg defects as distal as 6.6 cm
above the medial malleolus
Local Muscle flaps are not frequently used in lower leg, ankle and foot –
For defect that are small in size fasciocutaneous flap are better – better coverage without loss of function.
For large defects – free flaps are better.
Fasciocutaneous flaps are useful for reconstruction around the foot and ankle (the donor site always requires skin grafting).
Retrograde peroneal flap –
- Useful for ankle, heel, and proximal dorsal foot defects.
- Blood flow is retrograde.
- Similarly retrograde anterior tibial artery fasciocutaneous flap can be used.
- Both peroneal and anterior tibial artery can be isolated as a perforators (saving the main arteries).
Retrograde sural nerve flap –
Useful for ankle and heel defects.
Receives retrograde flow from a peroneal perforator 5cm above the lateral malleolus.
Artery first courses above the fascia and then penetrates deep to the fascia at mid-calf.
A common problem with the flap is venous congestion- problem with venous drainage.
Venous congestion – can be minimized if the pedicle is harvested with 3 cm of tissue on either side of the pedicle and with the overlying skin intact.
Venous congestion – can be minimized – if the flap is delayed, 4 to 10 days earlier, by ligating the proximal lesser saphenous vein and sural artery.
Inset of flap is critical to avoid kinking of the pedicle.
Splinting is necessary to avoid pressure on the pedicle.
Major donor deficit – the loss of sensibility along the lateral aspect of the foot.
Depression at donor site can be problematic if patient subsequently requires BK amputation.
Donor site deficit can be minimized if the flap is harvested as a perforator flap.
Supramalleolar flap –
- Used for lateral malleolar, anterior ankle, and dorsal foot defects.
- Harvested either with the overlying skin or as a fascial layer.
- Donor site can be closed primarily.
- Flap reach is limited, but can be expanded by applying delay approach.
Foot flaps –
Muscles in foot are – type 2.
Useful for coverage of relatively small defects.
Coverage of small mid- and posterior lateral defects of the sole of the foot and lateral distal and plantar calcaneus.
Dominant pedicle is medial to the muscle’s origin at the calcaneus and the muscle has a thin distal muscular bulk.
Larger muscle than ADM
Used to cover medial defects of the mid- and hindfoot, medial distal ankle.
Dominant pedicle – is at the takeoff of the medial plantar artery
Flexor digiti minimi brevis –
Used to cover defects over the proximal fifth metatarsal
lt receives its dominant pedicle at the lateral plantar artery takeoff of the digital artery to the fifth toe.
Flexor hallucis brevis –
Can be raised on a longer pedicle as an island flap on the medial plantar artery – can reach up to proximal ankle.
EDB muscle –
Very little bulk.
Can be used for local defect over sinus tarsi or lateral calcaneum.
Used to cover plantar heel defects.
Medial plantar flap –
Most versatile flap of the foot.
Ideal tissue for coverage of plantar defects.
It can also reach medial ankle defects.
Can be harvested to a size as large as 6 cm x 10 cm.
It is a sensate flap.
Has a wide arc of rotation if harvested till proximal part of medial plantar artery.
Flap can be raised on either of – deep or superficial branch of MPA.
Flap is easier to raise on deep branch, but raising the flap on superficial branch disturbs less of blood supply of foot.
When harvested with retrograde flow – it is based on the deep branch of the medial plantar artery.
Lateral calcaneal flap –
- Useful for postetior calcaneal and distal Achilles defects.
- Length of the flap can be increased by harvesting it as an L-shaped flap. L-shaped extension below and posterior to lateral malleolus.
- It is harvested with sural nerve and saphenous vein.
Dorsalis pedis flap –
- Can be either proximally or distally based
- Used for coverage of ankle and dorsal foot defects.
- Width of flap >4cm require skin grafting for closure
- Now rarely used – exposes vulnerable extensor tendons, and vascular structures.
Filet of the toe flap –
Useful for small forefoot web space ulcers and distal forefoot problems
Reach of the flap is always less than expected.
The technique involves removal of the nail bed, phalangeal bones, extensor tendons, flexor tendons, and volar plates while leaving the two digital arteries intact.
A variation is the toe island flap, where a part of the toe pulp is raised directly over the ipsilateral digital neurovascular bundle and then brought over to dose a neighboring defect.
Treatment Options –
Guiding principle – coverage of a wound should be performed as quickly and efficiently as possible.
Once the wound is clean and well vascularized – one of the following technique is used for reconstruction –
- Healing by secondary intention
- Wound closed primarily
- Split- or full-thickness skin graft and or neodermis is applied
- Local random flap is transposed or advance
- Pedicled or island flap
- Microvascular free flap
Biomechanics of foot should be taken care during reconstructive procedure – which may require- bone rearrangement, partial joint removal or fusion, or tendon lengthening or transfer.
Method of soft-tissue reconstruction depends on –
- Patient’s medical condition,
- Surgeon’s experience,
- Size of the wound,
- Vascular status of the foot.
- Exposed structures (tendon, joint And or bone), and
- Access to the wound (i.e., an ilizarov frame limits the access to the foot)
Any procedure chosen aims for – restoration of a biomechanically sound foot (to prevent recurrent breakdown).
No tendon, joint, or bone involved –> Simple coverage (secondary intention, delayed primary closure, or simple skin graft and/or neodermis).
Even some of the complex wound with exposed tendon, bone or joint can be managed by wound care and then simple coverage – With NPWT, granulation tissue forms over tendon, bone, or joints.
It is critical to immobilize the wound over a moving joint and to offload the wound (to prevent shearing forces from disrupting the healing process).
More than 85% of all wounds can be dosed by simple techniques, while less than 15% require flaps.
Delayed primary closure – is planned once edema has subsided. NPWT is helpful in reducing edema.
In some region wound may heal by simpler method but can result in problematic with normal activity – such as over a joint, plantar foot and posterior heel – soft tissue is a better option.
Most foot and ankle wounds – can be closed by skin grafting.
Healthy granulating bed is the necessary prerequisite for STSG.
If the granulation bed contains bacteria/biofilm – it should be removed before placing the skin graft.
Wound can be then pulse lavaged and then skin grafted with 1:1 meshing.
NPWT can be used on low continuous suction as a temporary dressing for the first 3 to 5 days – helps absorb excess fluid and ensure fixation of the skin graft to the underlying bed and minimizes possible skin graft-recipient bed disruption from shear forces.
Ideal graft donor site for a plantar wound is – the glabrous skin from the plantar instep.
Flaps for foot reconstruction should be accurately assessed – vascular pedicle should be dopplerable.
Local flaps are useful for coverage of foot and ankle defect because they only need to be large enough to cover the exposed tendon, bone, or joint while the rest of the wound is skin grafted.
Local flaps and their variation are most commonly used to cover lower leg and foot defect – because pedicled, perforator or free flaps are difficult to plan due to access problem in patient having external fixators.
Pedicled flaps are more difficult to dissect, have higher perioperative complication rate but equally good long-term success as free flaps.
Free flaps in the foot and ankle carry the highest failure rate of free flaps in any anatomic location – most probably because the anastomosis is near zone of trauma.
Postsurgical Care –
No weight bearing for 6 weeks if plantar surface is involved.
Offload specific parts.
Reconstructive options by location of defect –
Forefoot Coverage –
Toe ulcers and gangrene – limited amputation
Ulcer under metatarsal head causes –
- Principal abnormal biomechanical force is a tight Achilles tendon.
- Bony abnormality (plantar-prominent metatarsal head)
- Ulcer present without any abnormality
Patient cannot dorsiflex his or her foot with the knee bent or straight –> both the gastrocnemius and soleus portions of the tendon are tight.
If the patient can dorsiflex his or her foot only when the knee is bent –> only the gastrocnemius portion of the Achilles tendon is tight –> in this case gastrocnemius recession should correct the problem.
In addition the posterior capsule of the ankle joint may be tight.
Treatment require release of Achilles tendon and if it foot still does not dorsiflex then additional posterior capsular release is performed.
Release of the Achilles tendon –> forefoot pressure drops dramatically and if underlying bone is not involved forefoot ulcer within 6 weeks post release.
The lengthening of a tight Achilles tendon has decreased the ulcer recurrence rate in diabetics by half at 2 years.
Patient has normal ankle dorsiflexion, but bony abnormality causing planter ulcer –
Plantar-prominent metatarsal head –> the affected metatarsal head is elevated with osteotomies and internal fixation. The metatarsal head is shifted 2 to 3 mm superiorly –> pressure is relieved –> ulcer to heal by secondary intention.
Ulcer without any bony abnormality –
Small size – heals by secondary intention.
Large ulcer with metatarsal head and shaft involvement –> single metatarsal involved – Ray amputation.
If ulcers are present under several metatarsal –> pan-metatarsal head resection
If >2 toes with the accompanying metatarsal heads have to be resected –> then a trans-metatarsal amputation.
While doing trans- metatarsal amputation – maintain normal parabola of with the second metatarsal being the longest.
Equinus deformity can result –> to prevent this –> extensor and flexor tendons of 4th & 5th toe is tenodesed with the ankle in the neutral position and/or the Achilles tendon lengthened.
The most proximal forefoot/distal midfoot amputation is – Lisfranc amputation where all the metatarsals are removed. To prevent equinus deformity – anterior tibial tendon is split and lateral aspect inserted on to cuboid bone. Also, achillis tendon is lengthened.
Post-operatively foot is placed in neutral position, until wound heals.
Midfoot coverage –
Defect on medial aspect (non-weight bearing area) – treated with SSG.
Small defects – V -to-Y flap, the bilobed flap, the rhomboid flap, and the transposition flap, pedicled abductor hallucis flap medially or an abductor digiti minimi flap laterally.
Slightly larger defects – large V-to-Y flaps, random, large, medially based rotation flaps, pedicled medial plantar fasciocutaneous flap.
Larger defects – free muscle flaps covered by skin grafts.
Ulcers in midfoot are usually caused by Charcot collapse of the mid foot plantar arch –
If the underlying fragmented bone has healed and is stable (Eichenholz stage 3) à then the excess bone is shaved à the ulcer heals by secondary intention or is covered with a glabrous skin graft or a local flap.
If the midfoot bones are unstable (Eichenholz stage 1 or 2) à then bone is excised using a wedge excision and the arch reconstituted by fusing the proximal metatarsals to the talus and calcaneus.
Hindfoot Coverage –
Among the most difficult of all wounds to treat.
Usually also reflect severe vascular disease.
They are result of the patient being in a prolonged decubitus position.
Partial calcanectomy (preferably vertical) – can create soft tiisue to cover defect.
Collapsed bone or bone spur can cause ulcer – needs to be shaved.
Distally based V-to-Y flap or larger medially based rotation flaps.
Plantar heel defects – pedicled flaps –
- Medial plantar fasciocutaneous flap
- Flexor digiti minimi muscle flap
- Extended lateral calcaneal fasciocutaneous flap
- Retrograde sural artery fasciocutaneous flap
Large defect – free muscle flap with SSG.
Underlying bone – if osteomyelitis – bone needs to be debrided.
Hindfoot amputations –
Chopart – leaves an intact talus and calcaneus while removing the mid- and forefoot bones of the foot
Symes – tibia and fibula are cut just above the ankle mortise and the deboned heel pad is anchored to the anterior portion of the distal tibia to prevent posterior migration.
Symes amputation is done if –
- There is insufficient tissue to primarily close a Chopart amputation.
- There is insufficient arterial blood supply for a free flap, or
- If the talus and calcaneus are involved with osteomyelitis.
Dorsum of the Foot –
Most wound treated with – SSG
Small local flaps
EDB muscle flap works well for sinus tarsi defects.
Supramalleolar flap can be used over the lateral proximal dorsal foot.
Larger defect – free fasciocutaneous flap eg. Free radial forearm flap with palmaris tendon to reconstruct extensor tendons.
Ankle Defects –
If wounds granulating – SSG.
NPWT can be used to promote granulation.
Local flaps can be used to cover critical areas (tendon, bone or joint) while rest of area can be skin grfted.
Local flaps – rotation or transposition flaps based on posterior tibial and peroneal arterial perforators.
Pedicled flaps –
- Supramalleolar flap,
- Retrograde sural artery flap,
- Medial plantar flap,
- Abductor hallucis muscle flap,
- Abductor digiti minimi muscle flap,
- EHL, and
- EDB muscle flap.