Essential Questions For Surgical Intervention Of Diabetic Foot Infections

By Andy Meyr, DPM

Where Is The Infection Coming From?

     The pathogenesis of diabetic foot ulceration and infection has developed into an established science. The triad of neuropathy, ischemia and trauma in the diabetic foot are the sources of the disease process.1-5 It is of the utmost importance to recognize the influence of each of these factors in the initial workup. Sensory, motor and autonomic components of neuropathy all contribute individually to disease progression. One must recognize the differences between macrovascular occlusive disease and microvascular endothelial dysfunction separately in order to effectively define the degree of ischemia present in a patient. Repetitive microtrauma, as opposed to an acute traumatic event, can be a factor for disease prevention with early recognition.      Three frequent locations in terms of diabetic foot infection source are submetatarsal ulcerations, interdigital infections and direct foreign body penetrations. Each commonly leads to proximal infection progression as well as deep plantar space involvement. There are different anatomic paradigms that one must consider in terms of evaluating these locations.      Certainly, depth is one of these paradigms. Absolute depth measurements offer very little clinical information in comparison to a functional view of depth from the surgical layers of dissection. One should evaluate an infection in terms of whether it extends through the dermis, superficial fascia, deep fascia, musculotendinous structures or to the level of bone. From this general information, one can then identify specific anatomic structures as being within the path of the infection.      This layered approach leads into a separate anatomic paradigm, that of the plantar compartments. Researchers have extensively investigated structural foot compartments from both the views of diabetic foot infections and compartment syndromes. While no absolute consensus exists, with studies demonstrating anywhere from three to 10 plantar compartments, the concept is generally well established.1,6-9      For a basic muscular breakdown of the plantar compartments in the second dissection interval of the foot, see “An Overview Of Plantar Musculature By Compartment And Layer” below.6,10 Differentiation of the plantar foot into medial, central and lateral components is entirely derived from the plantar aponeurosis and its medial and lateral intermuscular septa. Distinct potential spaces are created by the thick, fibrous bands of the deep fascia.6,10 Investigation of an infection should include which plantar compartment has been violated once one has determined that the second dissection interval is involved.      Submetatarsal ulcerations commonly involve all anatomic layers to the level of bone. Those developing under the first metatarsal head communicate directly with the medial compartment. The flexor hallucis longus tendon is particularly at risk for proximal progression of the infection. Those ulcerations under the fifth metatarsal head communicate directly with the lateral compartment and often with the central compartment through the flexor tendons. Those ulcerations under the second, third and fourth metatarsal heads communicate directly with the central compartment.      Interdigital infections can quickly spread through both the first and second dissection intervals. Those that penetrate the second dissection interval quickly encounter the lumbrical and flexor tendons as well as the neurovascular structures of the respective digits. These structures put an originally superficial infection at great risk for plantar space involvement in the central compartment.      Those infections from penetrating foreign bodies offer a great variety in terms of their anatomic depth and compartment involvement. One should evaluate them on an individual basis.

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