An important underlying cause leading to diabetic foot problem is neuropathy. Sensory neuropathy leads to a loss of protective sensation. Foot trauma is unrecognised and leads to ulceration. The ulceration is often the portal of entry for bacteria, leading to cellulites and/ or abscess formation. Motor neuropathy can lead to asymmetric muscle atrophy, foot deformity (equines deformity) and altered biomechanics. This leads to areas of high pressure during standing or walking and repeated trauma that may go unrecognised because of sensory deficit. Autonomic neuropathy results in loss of sweating and dry skin that leads to cracks and fissures and a portal of entry for bacteria. Diabetes is also associated with an increased risk of peripheral arterial disease and it can be a major factor in non- healing of foot ulcerations.
Diabetic patients can have significant foot infection, with much less pain and no pronounced systemic inflammatory response. A high index of suspicion is therefore required to diagnose foot infection in patients with diabetes.
The skin of the foot is a highly specialized organ. The plantar skin consists of a complex array of fascia, fibrous septae and tangential shearing forces that occur during walking. The dorsal skin is bound to the underlying extensor retinaculum. Infection tracks along fascial planes and tendon sheaths. The location of a diabetic foot wound will usually lead surgeon to the underlying cause. An ulcer at the posterior border of the heel is usually the result of chronic pressure from prolonged contact with bedding, friction from rubbing against rough bed sheets and lack of elevation. An ulcer about the plantar foot is almost always due to i) excessive pressure and time between the foot and the contact surface, ii) neuropathy and iii) deformity of the foot ( equines contracture). Understanding the underlying cause will allow an effective wound care. The single best means of reducing pressure on the sole of the foot is to employ non- weight bearing of the involved limb through use of crutches or walker. This may not always be practical but effort should be made to emphasize compliance. Use of standard off- loading shoes are also recommended.
Pain in a neuropathic foot is usually related to an underlying infection. After a thorough surgical preparation, in the emergency room, to remove debris and allow proper evaluation, the wound is probed to determine its depth and tissues involved. Osteomyelitis should be considered if the wound is deeper than the dermis layer. Most patients with diabetes who present with a severe foot infection have chronically poor glycemic control, chronic anaemia, poor nutrition and deficient clinical care. Therefore, laboratory studies and necessary management is essential before embarking on active treatment.
An important initial step in treating limb threatening diabetic foot infection is to perform a timely and adequate surgical debridement. This entails surgical excision of all nonviable and/ or infected tissue. The plantar spaces are opened by longitudinal incisions with division of plantar fascia. When pus is present in flexor tendon sheaths, these are opened and drained. In order to appropriately evaluate the viability of the soft tissues and the underlying structures, surgical debridement should be performed without the use of a tourniquet. If there is exposed bone or suspicion of osteomyelitis, cultures are obtained of this tissue. Wound is irrigated and meticulous hemostasis achieved. Most diabetic foot infections are treated with an empirically selected antibiotic regimen until cultures and sensitivity are available . In a limb threatening infection or osteomyelitis, intravenous therapy should be initiated and followed if possible by oral agents. The use of topical antibiotics has a limited place as may produce the development of resistant strains of colonized surface bacteria.
A patient with diabetes may not give the typical history of claudication because of associated neuropathy or lack of activity. It is therefore important to evaluate the limb for peripheral arterial disease even in the absence of symptoms. If pedal pulses are not clearly palpable, further vascular studies are indicated. An ankle- brachial index (ABI) should be obtained.
There is a close association between peripheral arterial disease and coronary disease making then both a high risk for a traditional open bypass procedure. The endovascular options include percutaneous angioplasty with or without a stent . These procedures cab be performed under local anaesthesia and sedation and with a high rate of limb salvage .
The standard treatment of diabetic foot ulcer includes adequate off- loading of weight, frequent ulcer debridement , wound care, treatment of infection and revascularization of ischemic limb. This standard care in many controlled trials has resulted in healing of a number of foot ulcers. However, newer therapeutic modalities that can improve healing also need to be explored.
Despite recent advances in surgical and radiologic vascular techniques, a fair number of patients with critical limb ischemia are not eligible for a revascularization procedure. This is because of anatomic location of the lesion, the extent of the disease or extensive co-morbidity . No effective pharmacologic therapy is available and amputation is often the only option left. The cost of managing a patient after amputation has been estimated to be almost twice that of a successful limb salvage . Therefore, exploring new strategies for ischemic limbs is of major importance. Bone marrow derived progenitor cells have been identified as a potential new therapeutic target.
Normal wound healing is a intricate process involving various cell types, coordinated processes, and complex signaling interactions. In a diabetic wound , many of these responses to inflammatory mediators, matrix production, angiogenesis, and wound contraction have all been poor and contribute to delayed healing of a diabetic wound.
Cell - based therapy is an attractive approach for the treatment of wounds with multiple impairments. Mesenchymal stromal cells (MSCs) are the multipotent cells derived from stroma of bone marrow and other tissues. The local delievery of MSC to a diabetic wound might correct wound healing impairment both indirectly by reversing local growth - factor deficiency, and directly by improving wound contraction through interaction with the extracellular matrix. The decrease in wound size might have the potential to offset diabetic - related wound - healing impairment significantly.
In a randomized controlled trial in 28 diabetic patients with critical limb ischemia, Huang et al reported improvement in limb ischemia and foot ulcers. By far the most studies of cell therapy have used intramuscular implantation method or intraarterial injection. Progenitor cell- based therapy may have great clinical potential.
