Peripheral arterial occlusive disease is 4x more prevalent in diabetics than in nondiabetics. It tends to occur at an earlier age in diabetics, and the risk of disease increases with the duration of diabetes.

The calcification of atherosclerotic plaques in arteries of diabetic patients is more diffuse and occurs within the tunica media of the arteries, producing a lead pipe appearance on plain radiographs (as opposed to plaques in nondiabetic patients, which are patchy and occur in the tunica intima).

The arterial occlusion of the proximal large vessels is similar to that in nondiabetics; however, the macrovascular disease is more diffuse in diabetics distal to the popliteal trifurcation. Distal vascular procedures have proven to be helpful in diabetic patients.

Microvascular complications of diabetes (neuropathy, retinopathy, and nephropathy) and macrovascular complications (peripheral vascular disease, coronary artery disease, hypertension, hyperlipidemia, and cerebrovascular disease) together contribute to diabetic foot problems.

A detailed history should be obtained, including a history of smoking, hypertension, and hyperlipidemia. Patients with advanced disease will complain of claudication.

Pain due to vascular claudication is usually relieved with rest. However, ischemic foot pain can also occur at rest.

On physical examination, absent popliteal or posterior tibial pulses, thin or shiny skin, absence of hair on the foot or leg, thickened nails, and dependent rubor are all signs of vascular insufficiency.

Any patient with signs of advanced vascular disease (such as a history of claudication, nonhealing ulcers, or nonpalpable pulses) should be evaluated by a vascular specialist.

Noninvasive vascular tests include the ankle-brachial index (ABI) using Doppler ultrasound pressures, transcutaneous oxygen (TcpO2) measurement (oximetry), the absolute toe systolic pressure (plethysmography), Doppler waveform analysis, and segmental Doppler limb pressures and pulse volume recordings.

Arterial pressure readings can be falsely elevated due to rigid arterial calcification in diabetics, which may artificially raise the ABI to > 1.00. Despite that, an ABI of < 0.80 is generally considered abnormal and < 0.45 in a diabetic patient is suggestive of limb-threatening ischemia.

Absolute toe pressures may be more predictive of distal wound healing with toe systolic pressure < 45 mm Hg indicating poor wound-healing potential and < 30 mm Hg indicating critical limb ischemia.

Transcutaneous oxygen measurement < 20-30 mm Hg represents poor wound-healing potential.

When assessing Doppler waveform recordings, a triphasic waveform is normal. Biphasic (loss of reverse flow in early diastole) and monophasic waveforms suggest advanced occlusive disease. If lower extremity ischemia is strongly suspected, arteriography, magnetic resonance angiography, or computed tomography angiography should be performed to assess the vascular flow.

Peripheral neuropathy is the most common cause of diabetic foot complications. The presence of neuropathy (diabetic or otherwise) greatly increases the risk of complications from any surgery.

Diabetic neuropathy can involve the sensory, motor, and autonomic pathways.

Diabetic neuropathy has been estimated to occur in 58% of patients with longstanding disease, although 1 study noted that close to 80% of diabetic patients having surgery had some degree of neuropathy.

The earliest finding in diabetic neuropathy is vibratory and proprioceptive loss. Signs and symptoms are variable but include paresthesias, burning sensations, hyperpathia, and dysesthesias and usually reveal a symmetric sensory loss in a “stocking-glove” distribution.

Due to the loss of protective (pain) sensation, foot ulceration generally occurs by repetitive trauma in areas of high mechanical pressure.

The 5.07 (10-g monofilament) Semmes-Weinstein monofilament (SWM) test of 7-10 plantar foot sites is the recommended screening test for a patient at risk for ulcer formation due to loss of protective sensation. However, up to 10% of patients who pass the SWM test may still develop skin breakdown.

A simplified screening test has been described. If a patient cannot sense the touch of a 4.5-g/4.65 SWM when it is pressed under the 1st metatarsal head with just enough pressure to bend the filament, the patient should be considered at risk for ulceration.

Denervation of the eccrine and apocrine glands and arteries leads to abnormal thermoregulation and interference with the normal hyperemic response to infection.

There is decreased sweating and loss of skin temperature regulation, causing dry, cracked skin and fissure formation, which predispose to infection by allowing a portal for bacterial entry.

Autonomic neuropathy can also cause orthostatic hypotension; cardiovascular, urinary, and gastrointestinal problems; and erectile dysfunction. It may produce chronic venous swelling, usually requiring management with compression stockings.

Motor neuropathy can cause muscle weakness and intrinsic muscle atrophy in the feet. The resulting muscle imbalance leads to claw toe and other forefoot deformities.

Metatarsophalangeal hyperextension and a distally displaced fat pad accentuate pressure under the metatarsal heads with risk for ulceration.

Proximal interphalangeal flexion can cause pressure on the dorsum of the toe against the toe box of a shoe, and distal interphalangeal flexion can lead to increased pressure at the end of the toe, both common areas for ulceration.

Although the etiology remains unclear, diabetic patients with decreased sensation may experience neuropathic pain resulting from small nerve fiber injury or from injury to the central or peripheral nervous system.

Patients generally complain of burning or shooting pain that may be worse at night, and they may experience allodynia or anesthesia dolorosa.

Neuropathic pain can be treated with low-dose antidepressants (amitriptyline, duloxetine), anticonvulsants (gabapentin, pregabalin), analgesics (tramadol), or local topical agents (capsaicin cream, lidocaine).

Surgical decompression of lower extremity peripheral nerves has been reported to relieve pain and restore sensation, but this approach is controversial and should be considered experimental.

An insensate foot in poorly fitting shoes is one of the most common causes for a diabetic ulcer.

The optimal shoe is an extra depth shoe that will allow for a custom insole.

Footwear options include a shoe with a padded heel counter and a wide and deep toe box, Plastizote shoe, Carville sandal (most accommodating for forefoot and hindfoot deformity), deep walking shoe, wide sneaker, or custom-made shoe.

Insoles are the mainstay of long-term nonoperative management of the diabetic foot to decrease plantar pressure and must be made out of accommodative material. Insoles are generally custom molded with dual layers; the upper layer should consist of a soft polyethylene foam (Plastizote or Pelite), which is most effective in “force distribution” to protect the plantar skin.

As of April 1, 2004, the Medicare Therapeutic Shoe Bill covers 1 of the following for each diabetic individual (who qualifies under Medicare part B) in 1 calendar year: 1 pair of custom-molded shoes and 2 pairs of inserts or 1 pair of extra depth shoes and 3 pairs of inserts.

Diabetic foot ulcers are the most common diabetic foot complication, and foot infection is the most common reason for a diabetic hospitalization in the USA.

15% of diabetic patients will develop a foot ulcer during their lifetime. Diabetic foot ulcers precede 85% of nontraumatic lower extremity amputations and are generally preceded by the triad of neuropathy, deformity, and repetitive trauma.

The most common risk factor for developing a diabetic foot ulcer is peripheral neuropathy. Diabetic foot ulcers commonly occur in areas of structural deformity, forming over areas of bony prominences and high pressure.

The area of maximum soft tissue damage secondary to vertical stress and shear occurs at the edge of pressure application (“edge effect”).

Ulcers can be neuropathic or ischemic.

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  Neuropathic ulcers are caused by pressure or by shear forces and generally have a healthy bed of granulation tissue beneath a necrotic cap.

  
  
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  Ischemic ulcers with underlying vascular insufficiency are usually painful and generally have a necrotic base. Ischemic ulcers should be evaluated by a vascular surgeon for limb salvage.

Diabetic individuals with sensory neuropathy generally lack sensation to deep pressure or pain. Loss of protective sensation due to peripheral sensory neuropathy, combined with unaccommodated structural foot deformities, commonly results in unrecognized acute or repetitive foot trauma (most commonly due to inappropriate footwear), leading to the development of ulcers with a risk of infection and possible amputation (pressure + neuropathy = ulceration).

Widely used classification systems are based on wound depth and appearance.

Neuropathic ulcers are generally not painful, whereas ischemic ulcers are often painful.

Consider biopsy for a chronic nonhealing ulcer to rule out the possibility of a Marjolin ulcer (squamous cell carcinoma arising from a chronic wound) or malignant melanoma.

Assuming appropriate medical management to optimize the systemic diabetes, treatment strategy includes ulcer bed preparation, local wound care with wound dressings, and protection and offloading.

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  Ulcer bed preparation includes debridement of necrotic or infected tissue to viable margins and callus removal.

  
  
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  Local wound care

  
  
  
  
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    The most commonly used dressing is a normal saline moist to dry dressing, which acts to debride the superficial layer when removed.

    
    
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    Absorbents (alginate or Hydrofiber) can be used for exudative wounds.

    
    
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    Occlusive hydrocolloids, hydrogels, and debriding agents (including hypertonic saline gel) are appropriate for necrotic wounds. Foams can be used for exudative or necrotic wounds.

    
    
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    Collagen dressings can be used for granulating or necrotic wounds. Transparent films (Opsite, Tegaderm) are helpful for dry granulating wounds without exudate. Antimicrobial dressings, including iodine- and silver-impregnated dressings, have also been used.

    
    
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    Dressings with biologically active wound-healing agents may promote healing in wounds with reasonable healing potential, including those with a cellulose and collagen framework (Promogran), hyaluronic acid ester (Hyalofill), those that deliver platelet-derived growth factors [becaplermin gel (Regranex)], and those that apply living fetal foreskin cells (Apligraf, Dermagraft).

    
    
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    A negative-pressure wound dressing (vacuum-assisted closure technique) has also been used to successfully treat nonhealing diabetic wounds.

  
  
  
  
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  Protection and offloading include casts, removable CAM walkers (which can be wrapped to ensure compliance), splints, or orthoses.

  
  
  
  
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    Total contact casting (gold standard) is an effective method to heal plantar ulcers with a reported mean healing time of ~ 39 days. Total contact casts may decrease plantar pressure at the ulcer site by distributing force over an increased weight-bearing area, may reduce shear forces and vertical plantar pressures, can protect from trauma, can immobilize the ulcer edges, and can reduce edema.

    
    
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    Initially, the total contact cast should be changed every 5-14 days due to the potential for extreme changes in soft tissue swelling, and a poorly fitted cast may lead to skin abrasion. Initial non-weight-bearing status is preferred, although moderate early weight bearing only minimally reduces the time to healing of plantar ulcers and may improve patient compliance.

    
    
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    The most common complication of total contact casting is recurrent ulceration. Contraindications to total contact casting include active infection, arterial insufficiency, poor skin quality, and poor patient compliance.

    
    
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    Treatment for the “at-risk” foot (grade 0) involves patient education, regular clinical examination, accommodative footwear, and pressure-dissipating orthotics. When a structural deformity or prominence is present that cannot be accommodated by external modalities, deformity correction or removal of the bony prominence is recommended to prevent ulceration.

    
    
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    Grades 1 and 2 ulcers require debridement of the necrotic or infected tissue, local wound care, and offloading/pressure relief techniques (external or surgical). Dressings and topical treatment abet the healing process. Once the ulcer has healed, patients should use offloading devices to help prevent reulceration.

    
    
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    Surgery is indicated when external accommodative modalities are not successful. Achilles tendon lengthening may help reduce the recurrence of neuropathic plantar forefoot ulcers in patients with limited ankle dorsiflexion by reducing peak plantar forefoot pressures. A heel ulcer is the most difficult to manage and most commonly requires surgery.

    
    
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    Operative treatment is generally necessary for grade 3 ulcers and those with associated gangrene, which commonly require debridement of infected or gangrenous tissue with partial- or whole-foot amputation and culture-specific parenteral antibiotic therapy.

  
  

Wound infections may occur as a result of abnormal white blood cell function, poor nutrition and glycemic control, and the presence of peripheral vascular disease.

Antibiotics generally should not be used to treat a foot ulcer unless there are clinical signs of infection or underlying osteomyelitis. Infections related to superficial ulceration and cellulitis are most commonly caused by aerobic gram-positive cocci or occasionally by enteric gram-negative bacilli, which can be safely treated by a 1st-generation cephalosporin or clindamycin.

Diabetic deep wound infections with associated necrosis or gangrene are most commonly polymicrobial with both aerobic and anaerobic (“fetid foot”) organisms and can be initially treated with broad-spectrum antibiotics. Swab cultures of the ulcer or sinus tract are generally not reliable.

Whenever bone is exposed in an ulcer, it should be considered infected. Osteomyelitis in an ulcer should be treated by surgical resection of the infected bone, in whole or in part, with antibiotic therapy.

Soft tissue gas in a diabetic is most commonly caused by aerobic organisms or by mixed gram-negative rods, but Clostridium perfringens and necrotizing fasciitis, which is a surgical emergency, must be ruled out.