Practical Plastic Surgery

present in the wound is variable. In outpatients with localized and superficial infections, the culprit is usually a Gram-positive cocci such as Staphylococcus or Streptococcus. Deep ulcers and more advanced limb infections are usually polymicrobial. Organisms include Gram-positive cocci, as well as Gram-negative bacilli such as Escherichia coli, Klebsiella, Enterobacter, Proteus and Pseudomonas. Anaerobic flora such as

Bacteroides is also common.

Clinical Assessment

Assessment of the diabetic foot starts with a thorough history and physical examination as well as directed laboratory studies to assess the metabolic status of the patient. The foot exam is directed toward assessing the primary pathophysiological mechanisms of disease, namely vascular and neurological compromise, and a search for occult or advanced infection.

Vascular Exam

Assessment of vascular compromise is critical, as it defines the degree of ischemic change to the foot. Evaluation of the femoral, popliteal and pedal pulses may suggest the site of large vessel arterial compromise if present. Additionally, prolonged capillary refill time, dependent rubor, pallor on elevation and loss of foot hair are all signs of arterial compromise. Although sensibility and motor function should be a part of any vascular exam, impairment may be due to ischemia as well as neuropathic changes.

16 When distal pulses are absent or impaired, the ankle-brachial index (ABI) can assess the degree of large vessel perfusion to the extremity. These values can be helpful in determining the potential for wound healing. An ABI of 0.4-0.6 correlates with significant claudication and a 10%-40% chance of progression of disease to amputation or revascularization to prevent amputation. Most diabetics need an ankle pressure of at least 80 to 90 mm Hg to heal a digit or metatarsal amputation. However, the ABI must be interpreted within the context of the disease. Medial arterial calcinosis, frequently seen in diabetics, especially those with end-stage renal disease results in artificially inflated indices. Although calcification appears to spare the vessels of the toes, disease in this area can often limit the utility of toe pressures.

Segmental Doppler analysis can warn the clinician of arterial compromise in the background of an elevated ABI. An attenuated waveform indicates a proximal occlusion, whereas a normal waveform is suggestive of insignificant proximal disease. Although segmental Doppler waveforms and pulsed Doppler recordings are not affected by calcification, these are qualitative, not quantitative, measures. Also, the quality of the waveforms is affected by local edema, and cuff placement may be affected by ulceration. The hindrances the diabetic foot presents to these noninvasive tests can significantly limit the usefulness of these modalities. The clinician is encouraged to assess these values in the context of the disease state and physical exam.

When foot pulses are absent and ulceration present, large vessel disease can be assumed to be a significant component of the disease process. Ischemic ulcers are usually painful, superficial lesions with a rim of vascularized tissue and a necrotic center. Arteriography, or magnetic resonance angiography (MRA) of the pelvis and entire lower extremity will provide a road map for a planned bypass procedure. As the proximal leg and foot vessels are frequently spared in diabetics, extreme distal bypass is not an uncommon procedure. Judicious hydration and renal protective agents prior to infusion of IV contrast are suggested for diabetics with compromised renal function. Although arteriography is considered the gold standard in vascular imaging, MRA is a useful alternative, particularly in patients with compromised renal function.

Neurological Exam

The foot should be thoroughly inspected for signs of neuropathic disease. Claw-foot deformity or other changes representative of motor disease should be noted. High-risk areas such as the plantar surface of the metatarsal heads, the dorsal PIP joints and the tips of the toes are inspected for ulceration. The toes are also inspected for ingrown nails; the web spaces and the plantar surface of the foot are inspected for dry, cracked skin. Sensibility, which is usually impaired in a bilateral, symmetrical pattern is assessed. Vibratory sensation, typically lost first, may be tested with a 128-cycle tuning fork. Light touch, temperature and pain can be assessed with a cotton swab, warm and cool tubes, and a pinprick, respectively. Neuropathic ulcers, known as mal perforans ulcers, present as nontender ulcers found on the plantar contact areas, such as the metatarsal heads or under the heel. They have a deep, punched-out appearance with a hypertrophic callous formation at the edges.

Searching for Infection

A thorough search for ulceration, purulent drainage, crepitus, erythema and sinus formation should be part of the initial evaluation. Heavily calloused areas are unroofed and cultures taken from the base of all ulcers. All wounds are probed to determine if the lesion exclusively affects the superficial tissue or if the deeper planes are involved. The tissue surrounding the ulcer is compressed to express occult purulence. Osteomyelitis is a common complication of the diabetic foot disease and is

seen in up to 70% of diabetic foot ulcers. The presence of exposed bone in an ulcer 16 is associated with bony infection. This observation can be made visually or with a sterile probe. In addition, plain X-rays, 3-phase bone scans, labeled leukocyte scans,

CT and MRI may be used to assess osteomyelitis. Bone biopsy is the gold standard of diagnosis. It should be noted that the hallmarks of infection such as erythema and pain may be absent in the diabetic due to the sequelae of microvascular and neuropathic dysfunction. Even patients with deep abscesses may not present with expected fever, chills and leukocytosis. Uncontrolled hyperglycemia may be the only harbinger of an active infection.

Necrotizing fasciitis, an infection of the subcutaneous tissue and fascia, is a frequently missed condition affecting diabetics. Although not a common infection, it is a devastating disease that can rapidly result in large tissue loss, sepsis and death. Clinicians may mistake this disease with cellulitis, and the diagnosis of necrotizing fasciitis is not usually considered until the patient is floridly septic. The diagnosis is frequently missed because the skin often shows no evidence of deep tissue infection. Crepitus, cyanosis or bronzing of the skin should raise suspicion. Easy and painless introduction of a probing instrument into the necrotic subcutaneous space is highly suggestive of the diagnosis. A X-ray CT or MRI of the affected limb may show subcutaneous air. Fascial thickening and stranding may also be appreciated on CT. Affected patients should be taken emergently to the operating room for aggressive debridement of all infected tissue. Patients may require repeat debridements, which may ultimately lead to amputation.

Management of Diabetic Ulcers

Eradication of Infection

Foot infections in diabetic patients can rapidly produce a septic state or spread widely through the deeper planes of the foot, and therefore demand immediate intervention. Not all foot infections, however, require hospitalization. Superficial

infections may be treated with a first-generation cephalosporin, nonweight-bearing status on the involved extremity, and close follow-up. More commonly, patients present with ulceration or gangrene involving the deeper planes of the foot, including tendon and bone. These patients require immediate hospitalization, foot elevation, debridement and initial broad-spectrum antibiotics, which can be narrowed when wound culture results are complete. The duration of antibiotic therapy depends on clinical resolution of the infection. In the face of osteomyelitis, prolonged intravenous antibiotic therapy is required, usually for four to six weeks. The course may be curtailed if the infected bone is thoroughly debrided.

Abscesses and deep-space infections are promptly incised and drained. All necrotic tissue must be surgically debrided. In advanced infections, amputation may be necessary to allow for complete drainage and excision of all devitalized tissue. Although all necrotic tissue should be removed, care is taken to conserve as much viable tissue as possible. An overly aggressive approach to debridement can lead to higher amputations and problems during closure.

After debridement and drainage, the wound is followed closely to ensure appropriate healing and eradication of the infection. Wounds are kept moist and weight-bearing on the affected limb should be kept to a minimum. During convalescence, nutrition should be optimized and serum glucose levels strictly controlled. Progressive foot necrosis, in the face of optimal medical management and wound

care, may signify underlying ischemia or may be indicative of an undrained abscess.

16

Local Wound Care

There are several adjuncts to wound care that can maximize healing in these difficult wounds. Vacuum assisted closure (VAC) has revolutionized the management of a variety of wounds. Animal and human studies have shown an accelerated rate of granulation tissue formation and increased nutrient blood flow to the wound compared to saline moistened gauze. Early data on diabetic wounds report an accelerated rate of healing and decreased wound surface area, compared with saline-gauze dressing. The greatest strength of the VAC device is its ability to contract the wound, thereby decreasing its depth. The patient may then be spared a major reconstruction, with all its associated risks and morbidities. Disadvantages of the device include added cost and patient discomfort. We stress that VAC therapy does not replace debridement. This therapy should commence after adequate debridement has occurred. A more detailed discussion of this modality can be found in the VAC chapter.

Wet-to-dry gauze dressing, in conjunction with surgical debridement has been the standard wound treatment by which all others have been measured. There is some evidence in the literature that debriding agents such as hydrogels and collagen-alginate preparations may be more efficacious in the treatment of diabetic foot ulcers. Further research is required to define the optimal applications of these this emerging modalities.

Of the numerous clinical studies that have tested the efficacy of various growth factors for the treatment of chronic foot ulceration, only topical platelet-derived growth factor (PDGF) has shown significant improvement in healing the diabetic foot. Becaplermin gel, also known as Regranex, is the recombinant human PDGF isoform BB and the only growth factor licensed for the treatment of chronic, full-thickness diabetic foot ulcers. Due to its significant cost, ($300-$400 for a 30-gram tube), becaplermin is recommended only for well-perfused, chronic diabetic foot ulcers that have failed standard wound therapy.

Peripheral Vascular Surgery

After the infection is controlled and signs of systemic toxicity have resolved, attention should be focused on maximizing pedal perfusion. Macrocirculatory dysfunction, as well and an impaired inflammatory response, predisposes the diabetic foot to ulceration in the face of even moderate ischemia. Restoration of impaired inflow is essential for healing and limb salvage. Options include endovascular techniques (i.e., angioplasty and stenting), bypass grafting or a combination of the two. The procedure of choice should be tailored to each individual patient with regards to anatomy, comorbidities and operative risk. Details of the different interventions are beyond the scope of this chapter. The vascular surgery team will lead in this endeavor. Communication between the vascular and plastic surgeons is critical at this point if a reconstructive procedure is planned. For example, the vascular surgeon may not consider the fact that his target vessels in a bypass procedure may also serve as the site of anastomosis for a future free flap.

Offloading

Changes in the bony architecture of the foot create abnormal pressure points resulting in characteristic patterns of ulceration. By relieving the local stress created at these points, recurrence of the ulcer can be prevented and the reconstruction of the affected area may be protected. Redistribution of pressure can be achieved surgically (e.g., metatarsal head resection, arthrodesis, partial calcanectomy, or Achilles

tendon lengthening) or by custom orthotic footwear, tailored to evenly distribute 16 pressure to the dorsum of the foot. These custom-made orthotic devices made of plaster or fiberglass allow for distribution of pressure off the wound so that the patient can remain partially active while the wound heals. These devices may be worn at home. Some patients complain of discomfort from the device, but it is an effective means of protecting the foot from further damage while it heals.

Reconstruction

The reader is referred to the lower extremity reconstruction chapter for the various strategies used to cover foot defects. Reconstructive issues particular to the diabetic foot are discussed here. Prior to surgery, systemic and local infection, including osteomyelitis, should be eradicated. All necrotic tissue is debrided and local perfusion is optimized by peripheral bypass surgery and/or local wound care. The patient should be nutritionally optimized, and blood sugar tightly controlled. Lastly, the patient must understand the type of reconstruction planned and the measures required for complete wound healing. Patient compliance with postoperative care (e.g., leg elevation, no weight bearing, glucose control etc.) cannot be overstated. The convalescence phase may take several weeks and the patient should be aware of their role in protecting the wound.

Most foot ulcers, due to the inelasticity of the surrounding skin, are not amenable to primary closure. Skin grafts are not recommended to cover wounds over primary weight-bearing areas. Small, well-perfused, noninfected neuropathic ulcers can be repaired in a single-stage procedure that includes debridement, bony reconstruction (for offloading of the affected area) and primary closure using a random flap. Scarring around the wound secondary to chronic inflammation limits the reach, and therefore the use, of random flaps.

Wounds less than 3x6 cm with exposed tendons, joints or bone may be repaired with a local muscle flap. These flaps have the advantage of straightforward

Table 16.1. Commonly used local muscle flaps for various diabetic ulcers

dissection, with minimal donor defects and primarily closure. The procedure can be performed with regional anesthesia, minimizing anesthetic risk. Some of the commonly used local flaps for various diabetic ulcers are listed in Table 16.1.

Again, it should be noted that such procedures require a commitment from both patient and surgeon. Although a long-term salvage rate of 89% has been reported, an average hospital stay is 27 days, and the average time to wound healing is 125 days.

Larger defects or defects not within reach of local muscle flaps may be repaired with free flaps in selected patients. Free flap success rates are equivalent in diabetic and nondiabetic patients. However, the diabetic patient is usually more debilitated and has significant comorbidities, which may preclude free flap reconstruction.

16 Pearls and Pitfalls

Prevention of diabetic foot ulcers through proper education is one area in which primary care providers often fall short. The plastic surgeon should take an active role in educating diabetic patients on this topic. Patients should appreciate the importance of strict glucose control, smoking cessation and routine foot surveillance. Foot protection, meticulous foot care, with particular attention to the skin and nails, regular podiatry visits and warning signs of an at-risk foot should all be reviewed. Proper shoe selection and sizing is critical in prevention of disease and may require a custom-made device. Patients should know that this is a devastating but preventable problem and they are at the helm of influencing the course of their disease.

Previous ulceration puts the patient at risk for future ulceration. Every effort should be made to reduce abnormal pressure loading. Immobile patients should have appropriate cushioning and ulcer precautions. Mobile patients will benefit from custom-fitted footwear to minimize mechanical trauma.

Suggested Reading

1.Akbari CM, Macsata R, Smith BM et al. Overview of the diabetic foot. Sem Vasc Surg 2003; 16:3.

2.Attinger CE, Ducic I, Cooper P et al. The role of intrinsic muscle flaps of the foot for bone coverage in foot and ankle defects in diabetic and nondiabic patients. Plast Reconstr Surg 2002; 110:1047.

3.Bennett SP, Griffiths GD, Schor AM et al. Growth factors in the treatment of diabetic foot ulcers. Br J Surg 2003; 90:133.

4.Blume PA, Paragas LK, Sumpio BE et al. Single-stage treatment of noninfected diabetic foot ulcers. Plast Reconstr Surg 2002; 109:601.

5.Evans D, Land L. Topical negative pressure for treating chronic wounds: A systemic review. Br J Plast Surg 2001; 54:238.

6.Jeffcoate WJ, Harding KG. Diabetic foot ulcers. Lancet 2003; 361:1545.

7.Sumpio BE. Foot ulcers. New Eng J Med 2000; 343:787.

environment, the slightest trauma puts too great a demand on the cells in the region and a chronic, nonhealing ulcer is established. Fibroblasts migrate to the area and lay down fibrin, resulting in the characteristic “fibrin cuff ” seen in many ulcers of venous origin.

Classically, wounds are found in the “gaiter” distribution around the lower extremities and around the medial malleoli. Although not usually very painful, they can cause discomfort and even moderate pain in certain patients. Trophic changes including hair loss on shiny, indurated, scaly, erythematous skin. Deeper induration can present as panniculitis, followed by the fibrinous, exudative ulcers of venous stasis.

Arterial Disease

The traditional form of peripheral vascular disease, arterial insufficiency, results from the occlusion of vessels and prevention of forward flow of blood, leading to ischemia and tissue death. Typically this is a result of atherosclerosis of peripheral vessels and presents in the lower extremities. Embolic events and vasculititis (mentioned in the rare causes section of this chapter) are other less common causes of arterial disease and can also occur in the upper extremities as well. Risk factors for arterial insufficiency include: diabetes, smoking, hyperlipidemia, hypertension, obesity and age. Any artery along the course of the femoropopliteal distribution can be affected. If larger vessels such as the popliteal, peroneal or either the tibialis anterior or posterior are involved, severe tissue injury can be seen. Limited tissue damage will occur with more distal arterial involvement. Usually, ulcers in arterial disease occur

17 in the distal regions of the feet and toes up to the malleoli or on the shin. Typically presenting in men ages 50 to 70, patients will report symptoms such as

intermittent claudication, rest pain, pain with extremity elevation and disuse atrophy. Physical findings include asymmetric or absent distal pulses and doppler signals, temperature discrepancies between limbs, delayed capillary refill, audible bruits, skin color changes (mottled, dusky appearance) and an ankle-brachial index (ABI) less than 0.8.

Embolic phenomena are seen in patients with risk factors such as atrial fibrillation, atrial or ventricular thrombus (either left-sided, or right-sided with a patent foramen ovale), valvular vegetation, recent surgery or angiography, or more proximal vascular disease. Other causes include amniotic fluid, fat or bile emboli and intra-arterial injections of air or medication; however, these are much less common than emboli from a cardiac source or a more proximal plaque in the extremity. Embolic events and in situ thrombosis should be considered in hypercoagulable states such as in patients with a known or suspected malignancy or disorders of the coagulation system (e.g., lupus, protein c/s or antithrombin deficiencies). Embolic occlusion presents with acute and often painful distal symptomatology. When smaller vessels are affected, it is not uncommon to see distal finger or toe color changes and necrosis in the setting of palpable pulses. Finally, any patient who has a distal arterial embolism should undergo an echocardiogram to evaluate the heart and should be ruled out for an aneurysm (aortic, iliac or popliteal) as the sources of the embolus.

Diabetes

Though not a disease of the vascular system primarily, it is important to have an understanding of the role of diabetes in the lower extremity wound. At least 15% of diabetics will develop a chronic, nonhealing wound during their lifetime, and approximately 40% of these will have a component of peripheral vascular disease as a contributing factor. Furthermore, diabetic patients are at risk of arteriosclerosis of peripheral vessels at a younger age.

Many diabetic ulcers result from peripheral neuropathies leading to pressure ulcers. When the usual sensory signaling that control distribution of weight and pressure across a large surface of the skin is lost, micro-ischemic environments occur at the sights of prolonged pressure, leading to tissue death and bacterial invasion. Furthermore, it has been shown that there is impairment to neovascularization, prolonged inflammation and decreased wound repair in diabetic wounds. Combining these pathophysiologic changes with the tendency towards arterial occlusive disease in diabetics, a wound with multiple contributing factors can occur.

Rare Vascular Diseases

A subset of patients will present with a picture that does not fit one of the classic causes for vascular wounds or will describe a history that suggests one of the rare causes for wounds of vascular origin. The more common of these will be described, with a more extensive list present in Table 17.1. Due to the fact that the vasculitides comprise a broad group of different diseases, no one disease process explains the common final pathway of vessel wall inflammation. Immune complex disease, antibody-dependent cellular cytotoxicity (ADCC), endothelial activation and coagulopathy have been invoked in models of inflammatory disease of the vasculature.

The vasospastic condition known as Raynaud’s disease classically presents in a young woman after exposure to cold or after cigarette use. The patient reports paresthesias, and a typical triphasic pattern of color change is seen in the affected acral body part, progressing from blue to white to red. The disorder is thought to result from increased serotonin release or an imbalance in vasoactive prostaglandins, and is known as

Raynaud’s phenomenon when associated with one of a number of underlying diseases, 17 including lupus erythematosus, scleroderma or drug use. Treatment involves avoid-

ance of the instigating stimuli, the use of vasodilators such as calcium-channel blockers or serotonin antagonists and surgical debridement of any necrotic tissue.

Inflammatory vasculititis such as thromboangiitis obliterans (Buerger’s disease) or Wegener’s disease often present in younger patients. These conditions are characterized by the size of the vessels involved (large, medium or small vessel disease) and cause distinct cutaneous findings. Small-vessel vasculitis often presents with urticarial-like lesions and palpable purpura, while mediumand large-vessel vasculitis commonly results in livedo reticularis, purpura, necrosis and ulceration. End-stage renal disease can lead to a phenomenon known as calciphylaxis syndrome. The findings of hyperparathyroidism, hypocalcemia, hyperphosphatemia, hypertriglyceridemia and hypomagnesemia make up the metabolic derangement of this disorder. Patients

Table 17.1. Rare vasculitic diseases that may lead to lower extremity wounds

Small vessels Small vessel-leukocytoclastic vasculitis, microscopic polyangiitis, allergic granulomatosis (Churg-Strauss), Henoch-Schonlein purpura, essential cryoglobulinemic vasculitis, erythema induratum Bazum, livedo reticularis, livedo vasculitis and Sneddon syndrome

Medium vessels Polyarteritis nodosa, Kawasaki disease

Large vessels Giant cell arteritis (polymyalgia rheumatica, Takayasu arteritis)

Reproduced from: Mekkes JR et al. Causes, investigation and treatment of leg ulceration. Br J Dermatol 148:390; ©2003 with permission from Blackwell Publishing.

develop cutaneous calcium deposition typically in a trunk and limb girdle distribution, and go on to have painful full-thickness necrosis in these areas. Treatment involves correction of the metabolic changes and debridement and skin grafting once disease progression has been controlled.

Initial Workup

Following an interview aimed at understanding the history of the disease and the presence of risk factors for such things as embolic events or venous thrombosis, examination of the affected area follows (Table 17.2). The location of the wound may give the first clue as to the origin of disease. Venous stasis ulcers can often be diagnosed by the presence of edema, lack of hair, pigmentation changes from hemosiderin deposition and ulcers in a distribution around shin and calf regions. These findings may present so classically as to require no further work-up. A wound with an irregular border and black necrosis or with purple or reddish discoloration of surrounding tissue should raise the clinician’s suspicion for a vasculitis. A biopsy as well as lab test such as erythrocyte sedimentation rate, antinuclear antibody test, rheumatoid factor, antineutrophil cytoplasmic antibodies, and compliment and immune complex levels should be sent.

If arterial disease is suspected or if a compression dressing is to be applied, ABIs should be performed with the lower limit permissive for the use of compression dressings being above 0.8. This cutoff is set to avoid causing ischemic conditions in marginally viable tissue with the use of the compression dressing. If pressures appear

17abnormally high during this test, calcification of vessels preventing vessel occlusion during the test must be considered. This finding invalidates the ABI as a useful measure of arterial disease. Toe pressure measurement in the setting of inaccurate ABIs or in a patient with painful ulcers in the ankle region is another option. Further evaluation includes transcutaneous oxygen pressure measurement to evaluate the level of tissue ischemia, lower extremity color Doppler exam (as well as duplex scanning), and angiography (or MRA) for arterial occlusive disease.

In patients who present with evidence of peripheral neuropathies or ulcers over the sights of pressure points (especially the distal metatarsal joints) vibration perception (using a biothesiometer) and light touch sensation (using Semmes-Weinstein monofilaments) should be tested. Further workup for undiagnosed diabetes should include routine serum glucose and, if elevated, HbA1c levels should be checked.

Treatment

Wounds of Venous Etiology

Treatment for venous stasis ulcers is directed toward controlling lower extremity edema. Compression dressings create an external pressure which acts against the intravascular pressure to push plasma back into the vascular system and to prevent blood from pooling in the lower extremity. Options include a multilayer, zinc paste dressing bandage (the Unna boot), short stretch compression stockings and elastic bandages. There is no proven benefit of one over another; however the Unna boot should only be used in patients with good hygiene and minimal wound exudate. Compression stockings are often difficult to get on, especially for an elderly, arthritic patient. When dressing an extremity with the Unna boot, it is important to remember to wrap from distal to proximal and to avoid wrapping so tightly that the arterial flow is occluded. If using compression stockings, options include stockings graded from 20 mm Hg to greater than 60 mm Hg depending on the severity of disease.