Essential Questions For Surgical Intervention Of Diabetic Foot Infections

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A Guide To Intercompartmetal Communications

Medial Compartment
To the central compartment via:
-Adductor hallucis tendon
-Flexor hallucis longus tendon
-Peroneus longus tendon
-Neurovascular structures penetrating the medial intermuscular septum.
To the distal deep leg via:
-Flexor hallucis longus tendon

Central Compartment
To the medial compartment via:
-Adductor hallucis tendon
-Flexor hallucis longus tendon
-Peroneus longus tendon
-Neurovascular structures penetrating medial intermuscular septum
To the lateral compartment via:
-Long flexor tendon to fifth digit
-Short flexor tendon to fifth digit
-Lumbrical muscle to fifth digit
-Plantar interosseous muscle to fifth digit
-Peroneus longus tendon
-Neurovascular structure penetrating the lateral intermuscular septum.
To the distal deep leg via:
-Flexor hallucis longus tendon
-Flexor digitorum longus tendon
To the dorsum of the foot via:
-Interosseous muscles
-MPJ communications
To the plantar superficial fascia

Lateral Compartment
To the central compartment via:
-Long flexor tendon to fifth digit
-Short flexor tendon to fifth digit
-Lumbrical muscle to fifth digit
-Plantar interosseous muscle to fifth digit
-Peroneus longus tendon
-Neurovascular structures penetrating lateral intermuscular septum
To the dorsal structures
To the plantar superficial fascia

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Author(s): 
By Andy Meyr, DPM

     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.

Where Is The Infection Going?

     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

Where Will The Healing Come From?

     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.

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