TRUNK AND LOWER EXTREMITY
CHAPTER 95 FOOT AND ANKLE RECONSTRUCTION
CHRISTOPHER E. ATTINGER AND MARK W. CLEMENS
Functional restoration of the complex and efficient biomechanics of the foot and ankle is a challenge for the reconstructive surgeon. Trauma, tumor ablation, as well as changes in sensation, motor function, skeletal stability, blood supply, and immune status render the foot and ankle susceptible to breakdown. Inability to salvage the injured foot has traditionally led to amputation, carrying with it potentially dramatic morbid sequelae and a lifetime dependence on prosthetic devices. The relative 5-year mortality rate after major limb amputation in diabetics is greater than 50%, a startling figure when compared with mortality rates of lung cancer (86%), colon cancer (39%), and breast cancer (23%).
Successful foot and ankle reconstruction demands a team approach consisting of a vascular surgeon skilled in both endovascular and bypass techniques, a foot and ankle surgeon skilled in internal and external (Ilizarov) bone stabilization techniques, a soft-tissue surgeon for soft-tissue reconstruction, an infectious disease specialist, and a medical specialist to handle the comorbidities such as diabetes, hypertension, renal failure, and coronary artery disease.1 Surgical goals include a good local blood supply, debridement to a clean base, correction of any biomechanical abnormality, and nurturing the wound until it demonstrates signs of healing. Reconstruction can be accomplished by simple techniques 90% of the time and complex flap reconstruction in 10% of cases. This chapter focuses on the critical aspects of foot and ankle reconstruction, including anatomy, evaluation, diagnosis, and treatment with flap-based reconstructions.
The foot and ankle consists of six angiosomes2: (1) the distal anterior tibial artery feeds the anterior ankle while its continuation, the dorsalis pedis artery, supplies the dorsum of the foot; (2) the calcaneal branch of the posterior tibial artery feeds the medial and plantar heel; (3) the calcaneal branch of the peroneal artery feeds the lateral and plantar heel; (4) the anterior perforating branch of the peroneal artery feeds the anterolateral ankle; (5) the medial plantar artery feeds the plantar instep; and (6) the lateral plantar artery feeds the lateral plantar mid- and forefoot (Figure 95.1). Note that the plantar heel receives dual blood supply from both the calcaneal branches of the posterior tibial and peroneal arteries. When the heel develops gangrene, this usually implies severe vascular disease involving both the peroneal and posterior tibial arteries.
Because the foot is an end organ, many arterial–arterial anastomoses provide a duplication of inflow. These arterial–arterial anastomoses (Figure 95.2) provide a margin of safety if one of the main arteries becomes occluded. At the ankle, the anterior perforating branch of the peroneal artery is connected to the anterior tibial artery via the lateral malleolar artery. At the Lisfranc joint, the dorsalis pedis artery dives into the first interspace to connect directly with the lateral plantar artery. This vascular loop is critical in determining the direction of flow within the anterior or posterior tibial arteries, which can be antegrade or retrograde or both. In addition, the plantar and dorsal metatarsal arteries are linked to one another at the Lisfranc joint by proximal perforators and at the digital web spaces by distal perforators. Finally, the posterior tibial artery and peroneal artery are directly connected deep to the distal Achilles tendon by one to three connecting arteries. Using a Doppler ultrasound probe and selective occlusion, one can determine the patency of these connections as well as the direction of flow. This knowledge is critical in designing local flaps, pedicled flaps, and amputations.3
FIGURE 95.1. The angiosomes of the foot and ankle include (A) the anterior ankle fed by the anterior tibial artery and the dorsum of the foot fed by the dorsalis pedis artery; (B) the medial and plantar heel fed by the calcaneal branch of the posterior tibial artery, the plantar instep fed by the medial plantar artery, the lateral plantar midfoot and plantar forefoot fed by the lateral plantar artery; and (C) the anterolateral ankle fed by the anterior perforating branch of the peroneal artery and the lateral heel fed by the calcaneal branch of the peroneal artery.
FIGURE 95.2. Arterial anatomy of the foot and ankle. At the ankle, the anterior tibial artery gives off the lateral malleolar artery at the level of the lateral malleolus that anastomoses with the anterior perforating branch of the peroneal artery. At the Lisfranc joint, the dorsalis pedis artery dives deep in the first interspace to join the lateral plantar artery. At the second, third, and fourth proximal interspaces, the proximal perforators link the dorsal and plantar metatarsal arteries. Not shown is the direct connection between the peroneal and posterior tibial artery deep to the distal Achilles tendon. (From Attinger C. Vascular anatomy of the foot and ankle. Oper Tech Plast Reconstr Surg. 1997;4:183, with permission.)
Motor and Sensory Anatomy
The sciatic nerve divides into the tibial and common peroneal nerves proximal to the popliteal fossa. The tibial nerve runs lateral to the popliteal vessels within the popliteal fossa, before entering the deep posterior compartment of the leg. The tibial nerve innervates muscles of the deep and superficial posterior compartments (except the gastrocnemius muscle) and trifurcates at the distal inner ankle, deep to the flexor retinaculum, into the calcaneal and medial plantar and lateral plantar nerves. These nerves provide the motor branches to the intrinsic muscles of the foot (except the extensor digitorum brevis [EDB] muscle). The common peroneal nerve passes around the lateral aspect of the fibular head before splitting into the superficial and deep branches. The deep peroneal nerve innervates the extensor muscles in the anterior compartment before exiting the extensor retinaculum to innervate the EDB muscle. The superficial peroneal branch innervates the everting peroneal muscles of the lateral compartment before it pierces the fascia to become subcutaneous and provide sensibility to the lateral lower leg and dorsum of the foot.
FIGURE 95.3. Sensory innervation of the lower leg. Note that the sensory distribution of the deep peroneal nerve is limited to the first web space, whereas the superficial peroneal nerve provides sensibility to the dorsum of the foot. The posterior tibial supplies the sole of the foot and toes.
The sensory nerves to the foot and ankle (Figure 95.3) travel more superficially than the motor nerves, and their degree of function is a useful index to the localization of trauma. As mentioned, the superficial peroneal nerve (L4, L5, and S1) supplies the anterolateral skin in the upper third of the leg while descending within the lateral compartment. 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). The deep peroneal nerve (L4, L5, and S1) exits the anterior compartment deep to the extensor retinaculum to supply and ankle and midfoot joints, sinus tarsi, and the first web space. The sural nerve (L5 and S1), derived from both the tibial and common peroneal nerves, descends distal to the popliteal fossa in the posterior aspect of the calf along the course of the lesser saphenous vein. It provides sensibility to the posterior and lateral skin of the leg’s distal third, prior to passing between the anterolateral border of the Achilles tendon and the lateral malleolus in order to supply the skin of the dorsolateral foot and fifth toe. The skin of the medial half of the lower leg and dorsomedial portion of the foot is innervated by the saphenous nerve (L5 and S1), a cutaneous branch of the femoral nerve. The dorsum of the foot has communicating branches between saphenous, sural, superficial, and deep peroneal nerves, and thus there is often an overlap in their respective terminal areas of innervation. As mentioned, the posterior tibial nerve at the distal portion of the tarsal tunnel divides into three branches that supply the sole of the foot: the calcaneal branch (S1 and S2) supplies the medial aspect of the heel pad; the lateral plantar nerve (S1 and S2) supplies the lateral two thirds of the sole and the fifth and lateral fourth toes; the medial planter nerve (L4 and L5) supplies the medial one third of the sole and the first, second, third, and medial fourth toes. The medial and lateral plantar nerve can have an overlap in their respective zones with the saphenous and sural nerves, respectively.
Approximately 24 million or 7.8% of all Americans have documented diabetes mellitus and 15% of them eventually develop a foot ulcer during their lifetime. Almost 15% of the health care budget of the United States goes toward management of diabetes, with 20% of hospitalizations and 25% of diabetic hospital days for the treatment of diabetic foot ulcers. Two thirds all the major amputations performed per year in the United States are performed in diabetics. Diabetics battle numerous complications related to their underlying disease, but none is more devastating, both psychologically and economically, than gangrene of an extremity with the associated risk of amputation.
Diabetic peripheral polyneuropathy is the major cause of diabetic foot wounds. More than 80% of diabetic foot ulcers arise in the setting of neuropathy. The neuropathy is a consequence of chronically elevated blood sugar that causes vascular and metabolic abnormalities. Elevated intra-neural concentrations of sorbitol, a glucose by-product, are thought to be one of the principal mechanisms for nerve damage. Further damage can result when the damaged nerve swells within anatomically tight spaces such as the tarsal tunnel. The combination of nerve swelling and tight anatomic compartments leads to the “double crush syndrome,” which may sometimes be partially reversed with nerve release surgery.4 Unregulated glucose levels elevate advanced glycosylated end product levels that may induce microvascular injury by cross-linking collagen molecules. Decreased insulin levels, along with altered levels of other neurotrophic peptides, may decrease maintenance or repair of nerve fibers. Other potential causative factors of peripheral neuropathy include altered fat metabolism, oxidative stress, and abnormal levels of vasoactive substances such as nitric oxide.
Hyperglycemia also affects the body’s ability to fight infection by diminishing the ability of polymorphonuclear leukocytes, macrophages, and lymphocytes to destroy bacteria. In addition, the diabetic’s ability to coat bacteria with antibiotics is diminished, which further helps shield bacteria from phagocytosis. As a result of this impaired immune state, diabetics are especially prone toStreptococcus and Staphylococcus skin infections. Deeper infections tend to be polymicrobial, with gram-positive cocci, gram-negative rods, and anaerobes present. Postoperative complication rates correlate directly with the level of postoperative hyperglycemia.
In patients with neuropathy, non-healing ulcers precede 80% to 95% of amputations. Despite attempts to decrease the number of amputations in the United States by various strategies from improving glucose control to more widespread screening exams for impaired sensibility, the number of amputations has continued to increase from 54,000 in 1990 to 65,700 in 2006.Arterial disease present in diabetic patients is usually located in the infra-popliteal region and significantly increases the risk of ulceration and possible amputation. It is present in greater than 50% of diabetic foot ulcers. So, while peripheral vascular disease is frequently present, peripheral neuropathy is the primary cause of foot wounds in the diabetic population.
The neuropathic changes in the diabetic feet are a result of the neuropathy in the motor, sensory, and autonomic nervous systems. The loss of pseudomotor function from autonomic neuropathy leads to anhydrosis and hyperkeratosis. Fissuring of the skin results and facilitates bacterial entry with subsequent infection. The lack of sensibility over bony prominences and between the toes often delays the detection of these small breaks in the skin.
Charcot deformities (neuroarthropathy) of the joints of the foot occur in 0.1% to 2.5% of the diabetic population. When present, the tarsometatarsal joints are involved in 30%; the metatarsophalangeal joints in 30%; the intertarsal joints in 24%; and the interphalangeal joints in 4% of the time. The explanation for these degenerative changes is widely debated. One possible etiology is “neurotraumatic,” i.e., joint collapse from damage that has accumulated because of insensitivity to pain. A more recent proposed etiology is due to osteopenia triggered by abnormalities in the RANK/RANK-ligand/osteoprotegerin system.
The process probably begins with a ligamentous soft-tissue injury accompanied by synovitis and effusion. In the absence of pain perception, continued use of the extremity exacerbates the inflammatory process. Eventually distention of the joint capsule leads to ligament distortion, resulting in joint instability. Further activity causes articular cartilage erosion, with debris being trapped within the synovium. These changes are often accompanied by loss of dorsiflexion of the foot due to the loss of Achilles tendon flexibility, adding further stress on the arch of the foot.5 This combination of changes can then cause a collapse of the medial longitudinal arch, altering the biomechanics of gait. The normal calcaneal pitch is distorted, which in turn causes severe strain to the ligaments that bind the metatarsal, cuneiform, navicular, and other small bones forming the long arch of the foot. Heterotopic bone formation and eburnation of load-bearing surfaces frequently result.
These degenerative changes overload specific parts of the foot rather than allowing the normal weight transition from heel to midfoot to forefoot. The increased focal stress leads to ulceration, infection, gangrene, and limb loss if the process is not halted or compensated for in its early stages. Diagnosis of a Charcot foot is often missed as it often presents as a swollen foot that is misdiagnosed as a sprain. Erythema may further confuse this presentation, leading to a misdiagnosis of cellulitis.
The motor component of the neuropathy further contributes to Charcot deformities as the intrinsic foot musculature atrophies and becomes fibrotic. The resulting metatarsophalangeal joint extension and interphalangeal joint flexion produce excessive pressure on the metatarsal heads and the ends of phalanges. The loss of both the transverse and longitudinal arches of the foot exacerbates the unfavorable weight distribution across the midfoot and metatarsal heads.
Atherosclerotic disease is a common cause of non-healing foot ulcers, especially in combination with diabetes. Hypercholesterolemia, hypertension, and tobacco use are additional risk factors for atherosclerosis. Other causes of ischemia in the foot include thromboangiitis obliterans (Buerger disease, generally seen in young smokers), vasculitis, and thromboembolic disease. The etiology of the ischemia requires accurate diagnosis before treatment is initiated.
When discussing revascularization plans with the vascular surgeon, it is important to consider within which angiosome the ulcer is located. Failure to revascularize the affected angiosome can lead to a 15% or greater limb loss rate despite a patent bypass. If the affected angiosome is directly revascularized, wound healing increases by 50% and the risk of major amputation decreases fourfold.6 For ulcers on the dorsum of the ankle or foot, the anterior tibial artery or dorsalis pedis should be revascularized if possible. If the connection between the dorsalis pedis and the lateral plantar artery is intact, then a bypass to the posterior tibial artery is equally successful. For heel ulcers, revascularizing either the posterior tibial artery or peroneal artery is necessary. For mid- and forefoot plantar wounds, the posterior tibial artery should be chosen, although revascularizing the dorsalis pedis can be equally effective if the connection between the dorsalis pedis and the lateral plantar artery is intact. If the ideal vessel is not available, then revascularization should proceed with the understanding that there is a greater than 15% chance of failure.
When the patient with significant peripheral vascular disease presents with gangrene, the timing of revascularization versus debridement is critical. If there is stable dry gangrene without cellulitis, then the revascularization should proceed promptly but nonurgently. If the patient presents with wet gangrene with or without cellulitis, the wound should immediately be debrided. Revascularization should then be performed on an urgent basis as progressive gangrene will occur without new blood flow. After revascularization, wound closure should be initiated only when the wound shows signs of healing with the appearance of new, healthy granulation tissue and neoepithelialization. It takes anywhere from 4 to 10 days after a bypass and up to 4 weeks after endovascular surgery for the wound to develop maximal benefit from the revascularization.
Connective Tissue Disorders
The connective tissue disorders (e.g., systemic lupus, rheumatoid arthritis, and scleroderma) cause difficult-to-treat recalcitrant vasculitis ulcers. These ulcers are frequently associated with Raynaud disease, which causes distal vasospasm and cutaneous ischemia. Treatment frequently requires immunosuppressive drugs such as steroids and immunosuppressive agents to control the autodestruction of tissue. Until the optimal immunosuppressive regimen is determined, the wound will not heal. The wound-retarding effects of steroids used in the immunosuppressive therapy are mitigated with oral vitamin A (10,000 U/d while the wound is open). The use of topical vitamin A is also effective. Close coordination with the rheumatologist is necessary in the management of these most difficult of wounds.
In addition, almost half of patients with vasculitic ulcers also suffer from a coagulopathy leading to a hypercoagulable state. The most frequent abnormalities involve antithrombin III, Leiden factor V, protein C, protein S, and homocysteine. Consequently, a coagulation blood panel is obtained on these patients and if abnormalities exist, they are treated with appropriate anticoagulants and/or medications by the hematologist.
The treatment of these ulcers is principally medical. Once the abnormalities are identified and corrected, wound-healing adjuncts can help in healing the wound. Cultured skin and hyperbaric oxygen can be used to stimulate the formation of a healthy granulation bed. Patience is required in treating these wounds as less than half go on to heal, which can take as long as 24 months.7
EVALUATION AND DIAGNOSIS OF THE WOUND
The etiology of foot and ankle wounds is often traumatic, with the underlying pathology complicating the healing process. Accompanying disease processes include infection, ischemia, neuropathy, venous hypertension, lymphatic obstruction, immunologic abnormality, hypercoagulability, vasospasm, neoplasm, self-induced wound, or any combination of the preceding. The most frequent systemic comorbidities include diabetes, peripheral vascular disease, venous hypertension, and connective tissue disorders.
Evaluation of the patient with a foot wound or ulcer begins with a history and physical examination. Important points in the history include etiology, duration and previous treatment of the wound(s), comorbid conditions (diabetes, peripheral vascular disease, venous insufficiency, atherosclerotic disease, autoimmune disorders, radiation, coagulopathy, etc.), current medications, allergies, and nutritional status. It is also important to assess the patient’s current and anticipated level of activity. Limb salvage is usually indicated if the patient uses the leg in any way (including simple transfers) and if medically tolerated and technically feasible. However, if the limb is not going to be used, then strong consideration should be given to performing a knee disarticulation or above-knee amputation to cure the problem and minimize the risk of recurrent breakdown.
When performing the physical examination, one should avoid the temptation to go right to the wound and examine the entire body. The wound examination includes measuring the wound (length, width, and depth) and assessment of the types of tissue involved (i.e., epithelium, dermis, subcutaneous tissue, fascia, tendon, joint capsule, and/or bone). The most accurate way of determining bone involvement is if one can directly feel bone with a metal probe, which correlates 85% of the time with the existence of osteomyelitis.6 Diabetic ulcers with an area >2 cm2 have a 90% chance of underlying osteomyelitis regardless of whether the bone is probed at the base of the wound. The levels of tissue necrosis and possible avenues of spread of infection via flexor or extensor tendons are then determined. If cellulitis is present, the border of the cellulitis is delineated with a marker and the date and time are noted. This permits the clinician to immediately monitor the progress of the initial treatment despite the lack of bacterial culture results.
The vascular supply to the foot is then examined. If pulses are palpable (dorsalis pedis or posterior tibial artery), there is usually adequate blood supply for wound healing. If one cannot palpate pulses, a Doppler should be used. The Doppler ultrasound probe also allows the surgeon to evaluate the non-palpable anterior perforating branch and the calcaneal branch of the peroneal artery. It also helps determine the direction of flow along the major arteries of the foot to accurately assess local blood flow when designing a flap or amputation. A triphasic Doppler sound indicates excellent blood flow; a biphasic sound indicates adequate blood flow; and a monophasic sound warrants further investigation by the vascular surgeon. A monophasic tone does not necessarily reflect inadequate blood flow as it may reflect lack of vascular tone and absence of distal resistance.
If the pulses are non-palpable or monophasic, then noninvasive arterial Doppler studies are indicated. It is important to obtain PVRs (pulse volume recordings) at each level because arterial brachial indices are unreliable in patients with calcified vessels (30% of diabetics and all renal failure patients). Ischemia may be present if the PVR amplitude is <10 mm Hg. Obtaining arterial toe pressures yields further information because digital arteries are less likely to be calcified; if the toe pressure is <30 mm Hg, ischemia may be present. Tissue oxygen levels are also helpful in determining whether there is sufficient blood flow to the extremity. Tissue oxygen pressure levels <40 mm Hg suggest insufficient local blood flow to heal a wound. Skin perfusion pressure (Vasamed, Eden Prairie, MN) less than 50 mm Hg also indicates insufficient blood flow to heal. If the noninvasive tests suggest ischemia, an arterial imaging study is obtained to evaluate whether a vascular inflow and/or vascular outflow procedure is required. While bypass surgery remains the gold standard for revascularization, the less invasive endovascular techniques are very effective in treating stenosed or obstructed arteries by dilation, recanalization, or atherectomy with or without stenting. Combined endovascular and bypass techniques are also effective.
Sensory examination is performed with a 5.07 Semmes-Weinstein filament that represents 10 g of pressure. If the patient cannot feel the filament, protective sensation is absent, leading to an increased risk of breakdown. In addition, one of the following should be used: vibration using 128-Hz tuning fork, pinprick sensation, or ankle reflexes. Motor function is assessed by looking at the resting position of the foot and the strength and active range of motion of the ankle, foot, and toes.
The bone architecture is evaluated by looking at whether the arch is stable, collapsed, or disjointed. Bone prominence can occur with collapsed midfoot bones (cuboid or navicular bone with Charcot destruction of the midfoot), osteophyte formation, or abnormal biomechanical forces (hallux valgus, hammer toe, etc.). An x-ray series of the foot is required (anteroposterior, oblique, and lateral). The views of the lateral foot should be weight bearing. Calcaneal, sesamoids, and metatarsal head views may be necessary if local pathology is suspected. It is important to remember that the x-ray appearance of osteomyelitis lags behind the clinical appearance by up to 3 weeks. A magnetic resonance imaging (MRI) scan can help with earlier detection of osteomyelitis, as well as with differentiation between osteomyelitis and Charcot collapse. In general, bone scans are of no value in evaluation of osteomyelitis when there is an ulcer present because the bone under an ulcer will show increased uptake, regardless of whether or not osteomyelitis is present. However, if proximal spread of osteomyelitis along a long bone is to be ruled out, then a negative bone scan can be very useful.
Finally, the Achilles tendon is evaluated. If the ankle cannot be dorsiflexed 10° to 15° beyond neutral, the Achilles tendon is tight and is placing excessive stress on the arch in the midfoot and on the plantar forefoot during gait. This needs to be addressed orthotically or surgically so as to avoid excessive pressure that could lead to Charcot collapse or forefoot plantar ulceration.
Preparing the Wound for Reconstruction
The goal of treating any type of wound is to promote healing in a timely fashion. The first step is to establish a clean and healthy wound base. An acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing. If the wound is adequately vascularized, a clean base can be established with simple debridement and either immediate closure or covering the wound with a negative-pressure wound closure device for subsequent closure. A chronic wound is a wound that is arrested in one of the wound-healing stages (usually the inflammatory stage) and cannot progress further. Converting a chronic wound to an acute one requires correction of medical abnormalities (high blood sugar levels, coagulation abnormalities, changing or modifying drug therapy, etc.), restoration of adequate blood flow, administration of appropriate antibiotics if infection is present, and aggressive debridement of the wound. The debridement should also include removal of the senescent cells along the edge of the wound (3 to 4 mm of the wound edge). If the wound has responded to this therapy, healthy granulation should appear, edema should decrease, and neoepithelialization should appear at the wound edge. Negative-pressure wound therapy (NPWT)8 is a useful post-debridement dressing for the uninfected, well-vascularized wound because it accelerates the formation of granulation tissue while decreasing wound edema and keeping the bacterial countdown.
Measuring the wound area weekly is a useful way to monitor progress, as the rate of normal healing is a 10% to 15% decrease in surface area per week. Assuming the underlying abnormalities have been corrected (e.g., infection, ischemia, and edema) and the healing falls below the normal healing rate, topical growth factors, cultured skin, and/or hyperbaric oxygen can be applied alternatively or in combination.
Surgical debridement is the single most underperformed procedure in treating foot and ankle wounds and ulcers because of concerns of how to repair the resultant defect.9 Leaving dead or infected tissue or bone behind because of concerns about wound closure leads to persistent infection and further necrosis with the risk of possible amputation. Biofilm is present in over 90% of chronic wounds. Its presence further complicates the debridement as it penetrates every aspect of the wound and can be found up to 4 mm deep to its base because it spreads along the perivascular plane of arterioles feeding the wound bed. Biofilm can consist of up to 60 different bacteria species, of which a majority are anaerobic. Tissue containing clotted veins or arteries in dermis or subcutaneous tissue, liquefied fascia or tendon, and non-bleeding bone should all be debrided. Debridement should be considered complete only when normal bleeding tissue remains.
Using colors to guide the debridement is useful to judge how much to remove. Debriding until only normal red (muscle), yellow (fat), and white (bone, tendon, and fascia) colors remain is a very useful visual guide. In addition, painting the base of the wound with blue dye before starting the debridement and making sure that all the blue is removed during the debridement helps insure that the entire wound base has been adequately debrided. Injecting blue dye into a sinus tract or abscess allows the surgeon to follow the tract and identify the source of the sinus. The most effective debridement technique consists of removing thin layers of tissue in a sequential fashion until only normal tissue is left behind. This minimizes the amount of viable tissue sacrificed while ensuring that the tissue left behind is healthy.
The skeleton can usually be stabilized by splinting or corrected by application of an external fixator (monoplanar frame and Ilizarov frame). The Ilizarov frame provides superior immobilization, allows for bone transport, and minimizes the risk of pin track infection because of the thin wire pins. In addition, the Ilizarov device with footplate helps avoid jeopardizing any dependent reconstruction (i.e., heel and plantar foot) by suspending the foot until the reconstructed wound heals.
Deep uncontaminated tissue cultures pre- and post-debridement should be obtained during the initial and subsequent debridements to guide antibiotic therapy (both intravenous and topical). Effective dressings for wounds that may still harbor significant bacteria include topical antibiotics and/or biocides containing acetic acid, bleach, silver, or iodine. For heavily exudative wounds, an absorbent dressing with biocidal ingredients or NPWT should be used. For wounds that are clean and well vascularized, a moist dressing or NPWT can be applied. Debridement is rescheduled as frequently as necessary if there is progressive tissue necrosis or destruction or persistent positive wound cultures.
Biologic debriding agents such as maggots are useful in patients too ill for anesthesia or in patients awaiting revascularization. Maggots consume all bacteria including antibiotic-resistant bacteria such as VRE (vancomycin-resistant enterococci) or MRSA (methicillin-resistant Staphylococcus aureus) as well as biofilm.
After initial debridement to clean the tissue, it is important to select a therapeutic option to both prevent a subsequent buildup of metalloproteases that destroy naturally produced growth factors and prevent biofilm from reestablishing itself. The bacterial biofilm and proteinaceous debris that form on the wound surface must be removed at regular intervals. This can be done by scrubbing the wound daily or using wet-to-dry dressings. Dressings that absorb metalloproteases as well as destroy or inhibit biofilm need to be used as intermittent dressings. There is some evidence that polymerase chain reaction–guided topical antibiotic gel mixtures accompanied are also effective in controlling biofilm.10
If the wound fails to show signs of healing despite being clean and having adequate blood flow, it can often be converted into a healing wound by providing local wound-healing factors to the site. One can apply a platelet-derived growth factor (Regranex, Ortho-McNeil Pharmaceutical, Raritan, NJ) daily to the wound or place a sheet of cultured skin that produces the entire range of growth factors every 1 to 6 weeks (Apligraf, Organogenesis, Canton, MA; Dermagraft, Advanced Tissue Sciences, La Jolla, CA). The formation of new tissue also can be stimulated by placing a layer of inert dermis (Integra, Integra LifeSciences, Plainsboro, NJ) over a healthy wound bed and allowing it to revascularize over the next 10 to 12 days with NPWT or over 3 weeks without NPWT. The newly vascularized dermis can then be skin grafted with a thin autograft.
Finally, level-one evidence has demonstrated that systemic hyperbaric oxygen can also be used to convert a non-healing wound into a healthy granulating wound provided one follows approved indications for the procedure.11 Hyperbaric oxygen stimulates local angiogenesis in the wound bed, helps in the formation of collagen (cross-linking and extrusion from the cell), and potentiates the ability of macrophages and granulocytes to kill bacteria. When healthy granulation tissue appears, the wound can then be closed safely. Failure to wait until the wound has developed signs of healing (healthy granulation tissue, neoepithelialization at the skin edge, etc.) carries a high risk of failure.
Lower Leg, Ankle, and Foot: Muscle and Fasciocutaneous Flaps
Lower leg, ankle, and foot flaps are described, emphasizing their vascular supply and their indications. Further details of individual flap dissection are described in several atlases.12,13 More importantly, repeated cadaver dissection of these flaps, emphasizing the blood supply, is the most reliable way to become facile in their use.
Lower Leg and Ankle Flaps
The lower leg muscles make poor pedicled flaps because most of them are type 4 muscles with segmental minor arterial pedicles. As a result, only a small portion of the muscle can safely be transferred without a delay. Although the bulk of these muscles is small, the distal portion of some of these type 4 muscles (Figure 95.4) can be used to cover small defects around the ankle medially, anteriorly, and laterally. To successfully transfer a significant portion of the distal muscle, all the relevant minor perforators are preserved with the accompanying distal major artery and depend on retrograde flow. The sacrifice of a major artery should only be considered if all three arteries are open and there is excellent retrograde flow. It is important to tenodese the distal end of the severed tendon of the harvested muscle to a muscle with similar function so that the harvested muscle’s function is not lost. For example, if the distal muscular-tendinous portion of the extensor hallucis longus (EHL) muscle is harvested, the remaining distal EHL tendon should be tenodesed to the adjacent extensor digitorum longus so that hallux dorsiflexion is not lost. Because the loss of the anterior tibial tendon is so debilitating, this muscle should not be harvested unless the ankle has been or is being fused.
The EHL muscle can cover small defects that are as distal as 2 cm above the medial malleolus. The extensor digitorum longus muscle and peroneus tertius muscle are used for small defects as distal as 2 cm above the medial malleolus. The peroneus brevis muscle can be used for small defects as distal as 4 cm above the medial malleolus. The flexor digitorum longus muscle can be used for small defects as distal as 6 cm above the medial malleolus. The soleus muscle is the only type 2 muscle in the distal lower leg and so the minor distal pedicles can be detached and the muscle can be rotated with its intact proximal major pedicle rotated to cover large (10 cm × 8 cm) anterior lower leg defects as distal as 6.6 cm above the medial malleolus. It can be harvested as a hemisoleus for small defects and as an entire soleus for larger defects. These flaps require skin grafting. In addition, the ankle has to be immobilized to avoid dehiscence and ensure adequate skin graft take. External frames are useful for immobilization and NPWT assist in skin graft take.
FIGURE 95.4. The type 4 muscles of the lower leg are not only thin but can only be harvested for a distance of 2 to 3 segmental pedicles and therefore provide very little bulk to cover lower leg defects. The figure indicates how far proximal from the distal medial malleolus one can expect to find muscle to actually cover small lower leg defects. Fasciocutaneous flaps actually provide more bulk without affecting function. For larger defects a free flap is usually a better option. (From Attinger C. Plastic surgery techniques for foot and ankle surgery. In: Myerson M, ed. Foot and Ankle Disorders. Philadelphia, PA: WB Saunders; 2000:627, with permission.)
Fasciocutaneous flaps had their origin in 1981 when Ponten described the medial calf flap. Fasciocutaneous flaps are useful for reconstruction around the foot and ankle, although the donor site always requires skin grafting. The retrograde peroneal flap is useful for ankle, heel, and proximal dorsal foot defects. Its blood flow is retrograde and depends on an intact distal peroneal arterial–arterial anastomosis with either or both the anterior tibial artery and posterior tibial artery. The dissection is tedious and it does sacrifice one of the three major arteries of the leg. A similar retrograde anterior tibial artery fasciocutaneous flap has been described for coverage in young patients with traumatic wounds over the same areas. Because the anterior compartment is the only compartment of the leg whose muscles depend solely on a single artery, only the lower half of the artery can be safely harvested as a vascular leash. Both the peroneal and anterior tibial flaps can be dissected out as perforator flaps obviating the need to sacrifice a major vessel.
The retrograde sural nerve flap (Figure 95.5) is a versatile neurofasciocutaneous flap that is useful for ankle and heel defects. The sural artery travels with the sural nerve and receives retrograde flow from a peroneal perforator 5 cm above the lateral malleolus. The artery first courses above the fascia and then penetrates deep to the fascia at midcalf while the accompanying lesser saphenous vein remains suprafascial. The venous congestion often seen with this flap 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.Problems with venous drainage can be further helped if the flap is delayed, 4 to 10 days earlier, by ligating the proximal lesser saphenous vein and sural artery. The inset of the flap is critical to avoid kinking of the pedicle. Ingenious splinting is necessary to avoid pressure on the pedicle while the flap heals (the Ilizarov external frame can be useful in this regard). The major donor deficit of the flap is the loss of sensibility along the lateral aspect of the foot, while the skin-grafted depression in the posterior calf may pose a problem if the patient subsequently has a below-the-knee amputation. To minimize donor defect, this flap can be dissected out as a perforator flap.
The supramalleolar flap can be used for lateral malleolar, anterior ankle, and dorsal foot defects. It can be harvested either with the overlying skin or as a fascial layer that can be skin grafted. When harvested as a fascial flap, the donor site can be closed primarily. Various local or perforator flaps can also be designed over the row of perforators (Figure 95.6) originating from the posterior tibial artery medially and the peroneal artery laterally. Although the reach and size of these flaps are limited, both can be expanded by applying delay principle. These flaps are extremely useful in the closure of soft-tissue defects around the ankle in patients in an Ilizarov frame because accessibility to pedicled flaps or recipient vessels for free flaps can be problematic.
The muscle flaps in the foot have a type 2 vascular pattern and are useful for coverage of relatively small defects.14 The abductor digiti minimi muscle (Figure 95.7A) is very useful for coverage of small mid- and posterior lateral defects of the sole of the foot and lateral distal and plantar calcaneus. The dominant pedicle is medial to the muscle’s origin at the calcaneus and the muscle has a thin distal muscular bulk. The abductor hallucis brevis muscle (Figure 95.7B) is larger and can be used to cover medial defects of the mid- and hindfoot, as well as the medial distal ankle. Its dominant pedicle is at the takeoff of the medial plantar artery. Both of the above muscles can be used together to cover somewhat larger plantar defects in the midfoot and heel. The flexor digiti minimi brevis muscle is a small muscle that can be used to cover defects over the proximal fifth metatarsal bone. It receives its dominant pedicle at the lateral plantar artery takeoff of the digital artery to the fifth toe. The flexor hallucis brevis muscle has similar vascular anatomy, but can be harvested on a much longer vascular pedicle as an island flap on the medial plantar artery to reach defects as far as the proximal ankle.
The EDB muscle (Figure 95.8) has disappointingly little bulk but can be used for local defects over the sinus tarsi or lateral calcaneus. The muscle can be rotated either in a limited fashion on its dominant pedicle, the lateral tarsal artery, or in a wider arc if harvested with the dorsalis pedis artery. The flexor digitorum brevis muscle can be used to cover plantar heel defects. Because the muscle bulk is small, it works best if it is used to fill a deep defect that can then be covered with plantar tissue.
The most versatile fasciocutaneous flap of the foot is the medial plantar flap, which is the ideal tissue for the coverage of plantar defects. It can also reach medial ankle defects. The flap can be harvested to a size as large as 6 cm × 10 cm, has sensibility, and has a wide arc of rotation if it is taken with the proximal part of the medial plantar artery whether distally based on the superficial medial plantar artery or on the deep medial plantar artery (Figure 95.9). Although easier to harvest on the deep medial plantar branch, it is preferable to harvest the flap based on the superficial branch because there is less disturbance of the inflow to the remaining foot. When harvested with retrograde flow, the flap should be based on the deep branch of the medial plantar artery.
FIGURE 95.5. Retrograde sural artery flap. This flap depends on a peroneal perforator 5 cm proximal to the lateral malleolus. It also includes the lesser saphenous vein. Use of the flap sacrifices the sural nerve, leaving the lateral foot insensate. It is useful in covering lower leg, ankle, and hindfoot defects. A. Flap design. B. Flap dissection and arc of rotation. (From Attinger C. Soft tissue coverage for lower extremity trauma. Orthop Clin North Am. 1995;26:3, with permission.)
FIGURE 95.6. Location of the cutaneous perforators is shown. Perforators are shown as they emanate from the posterior tibial artery, peroneal artery, and anterior tibial artery. A flap designed with one of these perforators at its base, located by Doppler ultrasound probe, can encompass the territory fed by an adjoining perforator. To extend the flap successfully beyond those boundaries requires a delay procedure. (From Hallock J. Distal lower leg random fasciocutaneous flaps. Plast Reconstr Surg. 1990;86:304, with permission.)
The lateral calcaneal flap (Figure 95.10) is useful for posterior calcaneal and distal Achilles defects. Its length can be increased by harvesting it as an L-shaped flap posterior to and below the lateral malleolus. It is harvested with the lesser saphenous vein and sural nerve. Because the calcaneal branch of the peroneal artery lies directly on the periosteum, it is frequently damaged or cut during harvest.
FIGURE 95.7. Abductor digiti minimi and abductor hallucis brevis muscle flaps. These muscles have a type 2 vascular pattern, with the dominant pedicle at the level of the distal calcaneus. They are harvested on their dominant proximal pedicles. The distal muscle bulk is often disappointingly small. However, these muscles are useful to fill small midfoot, rear-foot, and distal ankle defects. A. Abductor digiti minimi. B. Abductor hallucis brevis.
FIGURE 95.8. The extensor digitorum brevis muscle is a small muscle based on the lateral tarsal artery that covers small defects over the anterior ankle and sinus tarsi. It can be harvested on its short dominant proximal lateral tarsal artery pedicle. Its reach can be extended by including the dorsalis pedis artery with either antegrade or retrograde flow depending on the location of the wound. (From Attinger C. Soft tissue coverage for lower extremity trauma. Orthop Clin North Am. 1995;26:3, with permission.)
The dorsalis pedis flap can be either proximally or distally based for coverage of ankle and dorsal foot defects. A flap wider than 4 cm usually requires skin grafting on top of the extensor tendon paratenon, which deprives the dorsum of the foot of durable coverage. Because the donor site is vulnerable from both a vascular and tissue breakdown perspective, the dorsalis pedis flap is now rarely used.
The filet of the toe flap is useful for small forefoot web space ulcers and distal forefoot problems, even though the 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. An elegant 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 close a neighboring defect, while its neurovascular pedicle is buried underneath the intervening tissue.
Reconstruction is guided by the principle that 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 reconstructive options is chosen: (a) the defect is allowed to heal by secondary intention; (b) the wound is closed primarily; (c) a split- or full-thickness skin graft and/or neodermis is applied; (d) a local random flap is transposed or advanced; (e) a pedicled or island flap is transferred; (f) a microvascular free flap is transferred. Biomechanics are a critical part of the reconstructive plan and may involve bone rearrangement, partial joint removal or fusion, or tendon lengthening or transfer. The method of soft-tissue reconstruction chosen hinges on the patient’s medical condition, the surgeon’s experience, the size of the wound, the vascular status of the foot, the exposed structures (tendon, joint, and/or bone), and the access to the wound (i.e., an Ilizarov frame limits the access to the foot). Any solution includes restoration of a biomechanically sound foot to prevent recurrent breakdown.
Simple coverage (secondary intention, delayed primary closure, or simple skin graft and/or neodermis) is recommended if there is no tendon, joint, or bone involved. Even more complex wounds involving exposed tendon, joint, or bone that mandated flap reconstruction in the past can now be treated with simpler methods. For example, wounds over the Achilles tendon easily develop adequate granulation tissue with good wound care and can be simply covered with a skin graft and/or neodermis. With NPWT, granulation tissue forms over tendon, bone, or joints that will heal either by secondary intention or be skin grafted. With neodermis, with or without the NPWT, a healthy dermal layer forms over tendon, bone, or joints that can be skin grafted with a thin autograft (Figure 95.11).15 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. Both NPWT and an external fixator can be used to minimize motion at the wound site, while the Ilizarov frame can be used to offload the wound (i.e., heel and plantar foot). Using these methods, more than 85% of all wounds can be closed by simple techniques, while less than 15% require flaps.
Wounds will frequently heal by secondary intention with daily dressing changes, application of the NPWT, and correction of the biomechanical abnormality. If the resultant scar might be problematic with normal activity (over a joint, plantar foot, and posterior heel), soft-tissue coverage may be the preferable option. A tight Achilles tendon is the principal cause of forefoot plantar ulceration in diabetics. By lengthening the tendon and applying a contact cast or equivalent, a plantar wound usually heals without further treatment over the next 6 weeks (see section on diabetic foot ulcers). The application of growth factor or cultured skin may hasten the process.
Delayed primary closure can be considered after the edema and induration of the wound edges have resolved. NPWT can be helpful in reducing the edema by absorbing all excess fluid. After primary closure, one should always check that relevant arterial pulses have not diminished because of an excessively tight closure. If the gap is too large to allow for immediate closure of the defect, the wound can be closed serially or the remaining gap can be left to heal by secondary intention. Adequate soft-tissue envelope can also be created by removing the underlying bone. This occurs in partial foot amputations where just enough bone is removed to develop adequate soft-tissue envelopes for delayed primary closure. Correcting the Charcot collapse of the midfoot arch by removing the arch and re-fusing the metatarsals to the hindfoot with the help of the Ilizarov external fixator usually allows for loose approximation of the plantar soft-tissue ulcer.
FIGURE 95.9. Medial plantar flap. The most versatile fasciocutaneous flap of the foot is the medial plantar flap. It is ideal for the coverage of plantar defects. It can be harvested on the superficial medial plantar artery or on the deep medial plantar artery. The flap shown is based on the deep medial plantar artery. A) The patient has a melanoma resected from his plantar heel. The medial plantar flap is drawn out on the plantar instep over the medial plantar artery. B) The medial plantar flap is dissected off of the instep. C) The medial plantar flap is elevated off of the instep. D) The healed wound shows a healed flap covering the plantar heel and the instep skin grafted.
FIGURE 95.10. Lateral calcaneus flap. This fasciocutaneous flap can be extended into an L shape so that it can cover part of the weight-bearing heel. The donor site is skin grafted. Part A shows the traditional non extended lateral calcaneal flap. Part B shows the design for the extended lateral calcaneal flap. (From Attinger C. Soft tissue coverage for lower extremity trauma. Orthop Clin North Am. 1995;26:3, with permission.)
FIGURE 95.11. Ankle ulcer. A. This large ulcer above the medial ankle was debrided to clean bleeding tissue and tibia. B, C. The wound was covered with a dermal regeneration template and NPWT for 10 days. D. The silicone sheet was removed off the now vascularized dermal template and a thin autograft was applied.
Skin grafting can be used to close most foot and ankle wounds. A healthy granulating bed is the necessary prerequisite. This can be achieved by the methods delineated above and include NPWT, cultured skin, growth factor, and/or hyperbaric oxygen. When there is a healthy granulating bed, neodermis can be applied to give a more solid construct on which to skin graft. Successful skin graft take is aided by removing the granulation bed that contains bacteria/biofilm before placing the skin graft. The wound is then pulse lavaged and new instruments are used to avoid recontaminating the wound base. The skin graft can be meshed at a 1:1 ratio to decrease the risk of seroma or hematoma although we prefer using an intact skin graft with perforations to allow trapped fluid to escape. The use of the NPWT 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.8 If the skin graft is over moving muscle or joint, it is critical to immobilize the foot and ankle by splinting or placement of an external fixator until the skin graft has completely healed.
The ideal graft donor site for a plantar wound is the glabrous skin from the plantar instep because the thicker glabrous skin graft resists the shear forces applied to the plantar foot during ambulation. It is harvested at 30/1,000th of an inch, meshed or perforated, and covered with NPWT. The donor site is, in turn, covered with a skin graft of 15/1,000th of an inch so that it heals rapidly and holds up better to the stress of ambulation. For plantar wounds where the patient is noncompliant either by choice or because of body habitus, consideration is given to placing an Ilizarov frame with a protective footplate until the graft has healed.
The use of any flap requires an accurate assessment of the blood flow. For local flaps, there should be a Dopplerable perforator close to the base of the flap. For pedicled flaps, the dominant branch to the flap should be patent. For perforator flaps, the perforator should be identified by Doppler and ideally visualized with duplex ultrasound. For free flaps, there should be an adequate recipient artery and vein(s). If there is any question, a duplex scan, CT or MRI angiogram, or normal angiogram is obtained.
Local flaps are useful in coverage of foot and ankle wounds 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. This frequently obviates the need for larger pedicled or free flaps (Figure 95.12). In addition, an infinite variation of local flaps can easily be done around or through an Ilizarov external fixator (Figure 95.13) because the lack of access makes pedicled, perforator, or free flaps hard to carry out.
FIGURE 95.12. V-Y flap. A, B. A V-Y flap is a V-shaped flap that, when advanced, forms a Y. C. The V-Y flap depends on the direct underlying perforators to stay alive. For that reason, the flap is dissected down through the fascial layer with no undermining. D. On the plantar aspect of the foot, the maximum advancement is limited to 1 to 2 cm.
Pedicled flaps in the foot and ankle area are often more difficult to dissect and have a higher perioperative complication rate, although equal long-term success, as free flaps.16 However, free flaps in the foot and ankle carry the highest failure rate of free flaps in any anatomic location and should be planned carefully. One reason for this is that complications arise when the anastomosis is performed at or near the zone of injury. In addition, the arteries are often calcified and special hardened micro-needles are often required. Anastomoses should be performed away from the zone of injury, either proximal or distal to the zone of injury, provided that the neurovascular bundle is intact. An end-to-side anastomosis to the recipient artery should be employed whenever possible to avoid sacrificing one of the main vessels to the foot. Two venous anastomoses are performed whenever possible to minimize postoperative flap swelling. The use of a coupling device for vein anastomoses speeds up the procedure.
The choice of free flap depends in large part on the length of pedicle needed. For long pedicles, the serratus, vastus lateralis, anterolateral thigh flap, radial forearm flap, and the rectus femoris muscles are excellent. It is important to remember that the pedicle can be extended by further dissection within the muscle belly. For the dorsum of the foot and ankle, thin fasciocutaneous and/or perforator flaps work best. For the plantar foot, skin-grafted muscle flaps and skin graft seem to hold up better than fasciocutaneous flaps with the normal wear and tear of ambulation.
Patients are generally not allowed to bear weight on the operated foot for 6 weeks if the plantar surface is involved. Appropriate devices can be prescribed to offload specific parts of the plantar foot: heel and forefoot. The help of a pedorthotist should be sought in cases where off-the-shelf offloading devices are not available. For dorsal wounds, patients are allowed to ambulate far sooner, provided they are in a dressing that protects the reconstruction. Because of these limitations, a patient will often need a course of physical and occupational rehabilitation to gain the strength and mobility to live independently at home. Patients should be followed closely in clinic during the postoperative period and should be seen by a pedorthotist to get the appropriate shoe to wear once they can bear weight. When healed, diabetics should return to the care of a podiatrist for preventive foot care.
RECONSTRUCTIVE OPTIONS BY LOCATION OF DEFECT
Toe ulcers and gangrene are best treated with limited amputations that preserve any viable tissue so that the amputated toe is as long as possible when closed. Attempts to preserve at least the proximal portion of the proximal phalanx should be made so that it can serve as spacer, preventing the toes on either side from drifting into the empty space. If the hallux is involved, attempts should be made to preserve as much as possible because of its critical role in ambulation.
FIGURE 95.13. Muscle flaps for ankle defects. Local flaps are particularly useful around ankle defects. They need only to be large enough to cover the portion of the wound that has exposed bone or tendons because the remainder of the wound can be skin grafted. A, B. In this instance, the tibio-talar junction could not be completely covered with a transposition flap. C–E. As a result, a abductor hallucis muscle flap and skin graft were harvested to cover the lower half of the wound.
Ulcers under the metatarsal head(s) occur because biomechanical abnormalities place excessive or extended pressure on the plantar forefoot during the gait cycle. Although hammertoes, long metatarsals, or sesamoids can be contributing factors, the principal abnormal biomechanical force is a tight Achilles tendon that prevents ankle dorsiflexion beyond the neutral position. 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. In addition, the posterior capsule of the ankle joint may be tight. A percutaneous release of the Achilles tendon is performed (Figure 95.14A and B), and if the foot still does not dorsiflex, then a posterior capsular release is performed. 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. A gastrocnemius recession should correct the problem (Figure 95.14C–E). The patient is kept in a contact cast or cam walker boot for 6 weeks. Because compliance in diabetics is as low as 28%, a cam walker boot is reinforced with casting material to ensure that it does not come off. With the release of the Achilles tendon, the forefoot pressure drops dramatically and the ulcer(s), if bone is not involved, heals simply by secondary intention in less than 6 weeks. The lengthening of a tight Achilles tendon has decreased the ulcer recurrence rate in diabetics by half at 2 years.5
For patients with normal ankle dorsiflexion who have a stage 1 to 3 plantar ulcer caused by a plantar-prominent metatarsal head, the affected metatarsal head can be elevated with preplanned osteotomies and internal fixation. The metatarsal head is shifted 2 to 3 mm superiorly. Upward movement with its attendant pressure relief is usually sufficient for the underlying ulcer to heal by secondary intention. The small, deep forefoot ulcers, without an obvious bony prominence, can be allowed to heal by secondary intention or with a local flap. For larger ulcers where the metatarsal head and distal shaft are involved, consideration is given to a partial ray amputation. Resecting the more independent first or fifth metatarsal causes less biomechanical disruption than resecting the second, third, or fourth metatarsal because the central three metatarsals operate as a cohesive central unit.
All efforts are made to preserve as much of the metatarsals as possible if more than one is compromised because they are important to normal ambulation. Local tissue is often insufficient in the forefoot and a microsurgical free flap is considered. If ulcers are present under several metatarsal heads, or if a transfer lesion from one of the resected metatarsal heads to a neighboring metatarsal has occurred, a pan-metatarsal head resection should be considered. If more than two toes with the accompanying metatarsal heads have to be resected, then a trans-metatarsal amputation is performed. The normal parabola, with the second metatarsal being the longest, is preserved. To avoid the resultant equinus deformity from the loss of the long and short toe extensors, the extensor and flexor tendons of the fourth and fifth toe should be tenodesed with the ankle in the neutral position and/or the Achilles tendon lengthened. As much plantar tissue as possible should be preserved to cover as much of the anterior portion of the amputation with healthy plantar tissue.
FIGURE 95.14. Achilles tendon lengthening. A. If both the gastrocnemius and soleus portion of the Achilles tendon are tight, the tendon can be released percutaneously by making three stab wounds at 2, 5, and 8 cm above the insertion of the Achilles into the calcaneus. A no. 15 blade is inserted into the central raphe of the tendon and the blade is turned 90° to cut half of the tendon at each site. The upper and lower cuts are in the medial direction and the center cut is in the lateral direction. B. Gentle dorsiflexion pressure is exerted on the foot until the tendon releases. C, D. If only the gastrocnemius portion of the Achilles tendon is tight, then a gastrocnemius recession can be done. The Achilles tendon is cut just below the muscle belly of the gastrocnemius muscles in a linear fashion while the soleus muscle remains intact. E. If the function of the gastrocnemius muscles is to be spared, then the cut can be made in a tongue-and-groove fashion.
The most proximal forefoot/distal midfoot amputation is the Lisfranc amputation where all the metatarsals are removed. The direction of the blood flow along the dorsalis pedis and lateral plantar artery is evaluated. If both have antegrade flow, then the connection between the two can be sacrificed. However, if only one of the two vessels is providing blood flow to the entire foot, the connection is preserved. To prevent an equinovarus deformity, the anterior tibial tendon should be split and the lateral aspect inserted into the cuboid bone. In addition, the Achilles tendon is lengthened. The Lisfranc amputation can be closed with volar or dorsal flaps, if there is sufficient tissue. If there is inadequate tissue for coverage, a free muscle flap with skin graft is used. Postoperatively, the patient’s foot is placed in neutral position until the wound has healed.
Defects on the medial aspect of the sole are non–weight bearing and are best treated with a skin graft. Ulcers on the medial and lateral plantar midfoot are usually caused by Charcot collapse of the midfoot plantar arch. If the underlying fragmented bone has healed and is stable (Eichenholz stage 3), then the excess bone is shaved via a medial or lateral approach while the ulcer heals by secondary intention or is covered with a glabrous skin graft or a local flap. For small defects, useful local flaps include the V-to-Y flap, the bilobed flap, the rhomboid flap, and the transposition flap. If a muscle flap is needed, a pedicled abductor hallucis flap medially or an abductor digiti minimi flap laterally works well. For slightly larger defects, large V-to-Y flaps; random, large, medially based rotation flaps; or pedicled medial plantar fasciocutaneous flap can be successful. Larger defects should be filled with free muscle flaps covered by skin grafts. Great care should be taken to tailor the flap so that it is inset at the same height as the surrounding tissue. If the midfoot bones are unstable (Eichenholz stage 1 or 2), then they can be excised using a wedge excision and the arch reconstituted by fusing the proximal metatarsals to the talus and calcaneus via an Ilizarov frame. The shortening of the skeletal midfoot usually leaves enough loose soft tissue to close the wound primarily or with a local flap.
Plantar heel defects or ulcers are among the most difficult of all wounds to treat. If they are the result of the patient being in a prolonged decubitus position, they usually also reflect severe vascular disease. A partial calcanectomy (preferably vertical) may be required to develop enough local soft tissue to cover the resulting defect. Despite sacrificing the Achilles tendon insertion, the patient can ambulate with a partially resected calcaneus provided they use accommodative foot orthoses. If there is underlying collapsed bone or bone spur causing a hindfoot defect, the bone should be shaved. These ulcers are usually closed with a large, distally based V-to-Y flap or larger medially based rotation flaps. Plantar heel defects can also be closed with pedicled flaps that include the medial plantar fasciocutaneous flap or the flexor digiti minimi muscle flap. Posterior heel defects are better closed with an extended lateral calcaneal fasciocutaneous flap or the retrograde sural artery fasciocutaneous flap. If the defect is large, then a muscle free flap with skin graft should be used. The flap should be carefully tailored so that there is no excess tissue and it blends well with the rest of the heel. Medial or lateral calcaneal defects usually occur after fracture and attempted repair. If osteomyelitis develops, the infected bone should be debrided and the defect filled with antibiotic-containing beads until the culture returns. Then, the medial defect can usually be covered with the abductor hallucis muscle flap medially or the abductor digiti minimi flap laterally. The exposed muscle is then skin grafted. After 6 or more weeks, the beads can be replaced with bone graft.
The two hindfoot amputations are the Chopart and Symes amputations. The Chopart amputation leaves an intact talus and calcaneus while removing the mid- and forefoot bones of the foot. To avoid going into equinovarus deformity, a minimum of 2 cm of the Achilles tendon has to be resected. When healed, a calcaneal-tibial rod can be used to further stabilize the ankle. The Symes amputation should be considered if there is insufficient tissue to primarily close a Chopart amputation and there is insufficient arterial blood supply for a free flap, or if the talus and calcaneus are involved with osteomyelitis. The 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. The large medial and lateral dog-ears can be carefully trimmed at the initial operation or 4 to 6 weeks later to yield a thin, tailored stump that can fit well into a patellar weight-bearing prosthesis.
Dorsum of the Foot
The defects on the dorsum of the foot are often treated with simple skin grafts. If the tissue covering the extensor tendons is thin or nonexistent, a dermal regeneration template (Integra) is applied and, when vascularized, covered with a thin skin autograft. Local flaps that can be used for small defects include rotation, bilobed, rhomboid, or transposition flaps. The EDB muscle flap works well for sinus tarsi defects and its reach can be increased by cutting the dorsalis pedis artery above or below the tarsal artery, depending on the presence of antegrade and retrograde flow and the location of the defect. The supramalleolar flap can be used over the lateral proximal dorsal foot and its reach can be increased by cutting the anterior perforating branch of the peroneal artery before it anastomoses with the lateral malleolar artery. For larger or more distal defects, the most appropriate microsurgical free flap is a thin fasciocutaneous flap to minimize bulk. The radial forearm flap is an excellent choice because it is thin, is sensate, and provides a vascularized tendon (palmaris tendon) to reconstruct lost extensor function. Thin muscle or fascial flaps with skin grafts are effective options as well.
Soft tissue around the ankle is sparse and has minimal flexibility. If there is sufficient granulation tissue, a skin graft will work well. To encourage the formation of a healthy wound bed, NPWT, with or without neodermis, can be used. The Achilles tendon, if allowed sufficient time to form a granulating bed, will tolerate a skin graft that will hold up well over time. Local flaps only need to cover the critical area of the wound including exposed tendon, bone, or joints while the rest of the wound can be skin grafted (Figure 95.13). Useful local flaps include rotation or transposition flaps based on posterior tibial and peroneal arterial perforators. Pedicled flaps include the supramalleolar flap, the retrograde sural artery flap, the medial plantar flap, the abductor hallucis muscle flap, the abductor digiti minimi muscle flap, the EHL, and the EDB muscle flap. Perforator flaps based on the posterior tibialis or peroneal artery can also be useful. Free flaps can either be fasciocutaneous or muscle with skin graft but they must be thin. To ensure good healing, the ankle should be temporarily immobilized with an external fixator.
Treatment of foot wounds requires, at a minimum, the presence of adequate blood flow, absence of infection, and a stable skeletal framework. A team approach is required. Once adequate blood flow has been verified or provided, debridement, the platform on which all reconstruction begins, is initiated. Debridement is aggressive and repeated as many times as necessary until the wound is ready for reconstruction. Reconstruction is only considered when the wound demonstrates signs of healing. Most wounds are closed with simple surgical techniques, and only a few require sophisticated anatomic knowledge to perform the necessary pedicled, perforator, or free flaps. Biomechanics are addressed in every patient so that recurrent breakdown is averted. Finally, when healed, appropriate orthotics and shoes are ordered to protect the reconstructed foot.
1. Sanders LJ, Robbins JM, Edmonds ME. History of the team approach to amputation prevention: pioneers and milestones. J Vasc Surg. 2010 September;52(3 suppl):3S-16S.
2. Attinger C, Evans KK, Bulan E, Blume P, Cooper P. Angiosomes of the foot and ankle and clinical implications for limb salvage: reconstruction, incisions, and revascularization. Plast Reconstr Surg. 2006;117:261S-293S.
3. Attinger CE, Cooper P, Blume P, et al. The safest surgical incisions and amputations using the angiosome concept and Doppler on arterial–arterial connections of the foot and ankle. Foot Ankle Clin North Am. 2001;6:745.
4. Dellon AL, Mackinnon SE. Chronic nerve compression model for the double crush hypothesis. Ann Plast Surg. 1991;26:259-264.
5. Mueller MJ, Sinacore DR, Hastings MK, et al. Effect of Achilles tendon lengthening on neuropathic plantar ulcers, a randomized clinical trial. J Bone Joint Surg Am. 2003;85a:1436.
6. Neville RF, Attinger CE, Bulan EJ, Ducic I, Thomassen M, Sidawy AN. Revascularization of a specific angiosome for limb salvage: does the target artery matter? Ann Vasc Surg. 2009;23(3):367-373.
7. Shanmugam VK, Price P, Attinger CE, Steen VD. Lower extremity ulcers in systemic sclerosis: features and response to therapy. Int J Rheumatol. 2010;2010. doi:pii: 747946. Epub August 18, 2010.
8. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical experience. Ann Plast Surg. 1997;38:563-576.
9. Steed DL, Donohoe D, Webster MW, et al. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. J Am Coll Surg. 1996;183:61-64.
10. Dowd SE, Wolcott RD, Kennedy J, Jones C, Cox SB. Molecular diagnostics and personalised medicine in wound care: assessment of outcomes. J Wound Care. 2011 May;20(5):232, 234-239.
11. Löndahl M, Katzman P, Nilsson A, Hammarlund C. Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care. 2010 May;33(5):998-1003.
12. Strauch B, Vasconez LO, Hall-Findlay EJ, Lee BT. Grabb’s Encyclopedia of Flaps: Volume III: Torso, Pelvis, and Lower Extremities. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
13. Wei FC, Mardini S. Flaps and Reconstructive Surgery. London: Saunders; 2009.
14. Attinger CE, Clemens MW, Ducic I, et al. Chapter 21: The use of local muscle flaps in foot and ankle reconstruction. In: Dockery GD, ed. Lower Extremity Soft Tissue & Cutaneous Plastic Surgery. 2nd ed. Kidlington: Elsevier Science; 2011.
15. Iorio ML, Goldstein J, Adams M, Steinberg J, Attinger C. Functional limb salvage in the diabetic patient: the use of a collagen bilayer matrix and risk factors for amputation. Plast Reconstr Surg. 2011 January;127(1):260-267.
16. Ducic I, Attinger CE. Foot and ankle reconstruction: pedicled muscle flaps vs. free flaps and the role of diabetes. Plast Reconstr Surg. 2011 July;128(1):173-180.