Dedicating oneself to the side of limb salvage in the fight against diabetic foot disease is a demanding and personally challenging enterprise. In the face of infection, it often seems as though all variables are against the surgeon and the patient as they both struggle against the possibilities of proximal amputation and limb loss. In fact, it often appears as though the only constant is the unpredictability of the disease progression.
However, expert knowledge in lower extremity anatomy is one of the most valuable tools that one can have in this fight. This knowledge allows one to answer the following key questions:
• Where is the infection coming from?
• Where is the infection going?
• Where will the healing come from?
Answering these three questions in the preoperative patient evaluation will assist in completing a planned, appropriate debridement as opposed to an aggressive but destructive procedure with little hope of viable outcome.
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.
Infections tend to develop and travel along the path of least resistance. This implies that an infection will stay within the potential space of a given surgical layer or plantar compartment before extravasation into another layer or compartment. Often this involves proximal extension along the relatively avascular tendon sheaths or fascial planes between muscular layers.
The studies that have helped define the number and boundaries of plantar foot compartments have also given us information about relatively consistent fascial clefts where communication between different layers and compartments is likely. These have involved pressurized injection imaging studies in which a contrast medium infiltrates a known compartment and one can map the extravasation into other compartments. The findings of these studies are summarized in “A Guide To Intercompartmental Communications” below.7,8,11-15
These communications are obviously numerous and complex. The important concept to realize is that an infection is likely to develop initially within the potential space of a single layer or compartment. There is a tendency for the infection to move proximally before communicating with another layer or compartment. However, note that patterns of communication are present along known anatomic structures such as tendons and neurovascular structures to each of the other compartments, as well as the dorsum of the foot and plantar superficial fascia.16 Intraoperative investigation of an infection should focus on these structures to trace the extent of plantar involvement.
Also note the majority of these communications are found in the forefoot around the metatarsophalangeal (MPJ) level so distal infections have an increased likelihood of multi-compartment involvement.11
One of the most important lessons the podiatric surgeon can learn is that we do not cure diabetic foot infections. No degree of surgical intervention will actually cure the patient of an invading pathogen. While aggressive surgical debridement will bluntly remove affected tissue, it will not continue to fight remnant infection and it will not heal remaining viable tissue. The patient’s own immune system is required for this with the vascular system as the necessary vehicle. For this reason, a thorough understanding of lower extremity angiosomes is essential in preoperative planning.
One cannot overstate the impact of vascular disease on diabetic foot infection. It is vitally important to have a thorough understanding of patients’ vascular status in terms of both macrovascular occlusive disease and microvascular endothelial dysfunction. Standard noninvasive vascular examinations and a formal vascular surgery consultation will provide preliminary information about this and help to optimize this system.
Surgeons need to take it a step further in order to garner specific information about which vessels are actually carrying blood into the foot and the collateral circulation. This is information that is readily available with a thorough physical examination using angiosome principles.
The term angiosome describes all tissue contained within the surgical layers of dissection supplied by a single source artery. There are five angiosomes in the foot and ankle, and they are supplied by the posterior tibial, anterior tibial and peroneal arteries. One can determine angiosome patency in the presence of macrovascular occlusive disease in the area of infection via a complete physical examination with a handheld Doppler. This information is vital in terms of incision placement, systemic antibiotic tissue penetration and the overall healing potential of infected sites.17-19 Thorough knowledge of angiosome principles is strongly encouraged for any surgeon undertaking diabetic limb salvage.
Diabetic foot surgeons do not cure infection. Our ultimate goal is facilitating healing through our surgical intervention, treatment and education. This is a challenging field that is only going to get more difficult in the future. With so many variables against us, we need to take advantage of those factors that we have some control over.
Expert knowledge of lower extremity anatomy is one of those factors that can have a true positive impact on patient outcomes if one applies this knowledge appropriately during the preoperative planning. Ask yourself the three questions of “Where?” the next time you encounter a diabetic foot infection.
Dr. Meyr is affiliated with the INOVA Fairfax Hospital Podiatric Surgical Residency Program in Falls Church, Va.
Dr. Steinberg is an Assistant Professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, D.C. He is a Fellow of the American College of Foot and Ankle Surgeons.
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