AJM Sheet: Imaging in Diabetic Foot Infections

AJM Sheet: Imaging in Diabetic Foot Infections

-Soft Tissue: Infection characterized by radiolucent area. One should be able to see a soft tissue deficit if an ulcer is present. It is very important to rule out emphysema (gas in the tissues) with a plain film. Can also appreciate soft tissue edema.

-Osseous Tissue:

-Early Osteomyelitis (OM) signs: No reliable ones. Rarefaction and periostitis are possible.

-Subacute OM signs: Brodie’s abscess (lytic lesion surrounded by sclerotic rim).

-Chronic OM: Lysis, Malformation, Involucrum, Cloaca, Sequestra.

-Plain film radiographs are 67% specific, 60% sensitive for OM [Termaat, JBJS 2005]
-MRI

-Cellulitis: T1: Diffuse and infiltrative decreased signal intensity as inflammation replaces fat.

-Note that pus/necrotic tissue has a decreased intensity compared to inflammatory fluid.

-Increased signal intensity in known OM indicates healing as fat infiltrates.

-Rim sign: thin layer of active infection surrounding normal bone.

-60% Specificity, 85% sensitivity per Termaat.
-Bone Scans

-A radio-isotope is injected into the patient and imaged at specific intervals.

-Phases: -Immediate Angiogram (1-3sec): Essentially an arteriogram.

-Blood Pool (3-5min): Demonstrates blood pooling in capillaries and veins.

-Delayed (2-4 hours): Increasingly specific to activity patterns and pathology.

-4^th Phase (varying times): Increasingly specific to activity patterns and pathology.

-Binds to calcium hydroxyapatite and measures osteoblast/osteoclast activity.

-Half-life: 6 hours

-Excreted through kidneys which will show homogenous control signal.

-Mucomyst 600mg PO q12 day before and of surgery as renal ppx.

-Cellulitis: Focal uptake in blood pool; Negative in delayed phase.

-OM: Diffuse uptake in blood pool; Hot increased uptake in delayed phases.

-45% Specificity; 86% sensitivity per Termaat.

-Same principles and phases as bone scan, but WBCs are tagged and followed instead.

-Uptake by siderophore complex (direct bacteria) and lactoferrin (protein-released by bacteria)

-Scan taken 48-72 hours after injection or done in triphasic manner.

-Has longer half-life

-42% Specificity; 80% Sensitivity per Termaat.
-Indium-111 Oxime

-WBCs isolated from blood sample, labeled and re-injected.

-Scan at 24 hours. Half life: 67 hours.

-Predominantly uptaken by neutrophils, so it demonstrates acute infections better than chronic infections.

-WBCs isolated from blood samples, tagged and re-injected. Scan at 3 hours.

-Tagged molecule is HMPAO (hexamethylpropyleneamine oxime  you will get asked this!)

-Technically easier with less radiation than indium.

-Specific for bone marrow and neutrophil production

-Has shown promise in differentiating OM from Charcot
-Combination Sequential Technetium-Gallium Scans

-Scan at 4 hours, then at 48-72 hours. Based on half-lives.

-Increased specificity for infection if gallium has higher uptake then technetium.

-Can use any other combination.

-Radiograph altered by computer to highlight specific “windows”. You can isolate soft tissue or different aspects of bone, for example.

-Soft tissue infection: Exact locations and anatomy of abnormal soft tissue density.

-OM: Increased density in the marrow.

-CT scans can be combined with contrast.
-Positron Emission Tomography (PET scans)

-A tracer is injected/inhaled into the patient which releases radioactive positrons. The positrons collide with electrons and produce gamma rays.

->90% Sensitivity and Specificity per Termaat (best in study).

AJM Sheet: Diabetic Foot Ulcer Pathogenesis

-The pathogenesis of the diabetic foot ulcer can be described via three mechanisms: neuropathy, trauma and impaired healing.

-30-50% of diabetics have some form of sensory, motor and/or autonomic neuropathy.

-Sorbitol accumulation in Schwann cells leads to hyperosmolarity of the nerve cells in turn leading to swelling and cellular lysis. This leads to decreased nerve signal conduction. Microvascular damage to the nerve (described later) also impairs healing of the damaged nerve.

-Sensory Neuropathy

-Loss of light touch/protective sensation (anterior spinothalamic tract)

-Loss of vibratory/proprioception mechanisms (posterior tract)

-Loss of pain/temperature sensation (lateral tracts)

-The patient has no warning of current, developing or impending trauma.

-Motor Neuropathy

-“Intrinsic Minus” foot-type with wasting of the intrinsic muscles and extensor substitution.

-Undetected excess plantar pressures develop.

-Autonomic Neuropathy

-Damage occurs in the sympathetic ganglion

-AV shunting occurs with global LE edema not relieved by diuretics or elevation.

-Increased skin temperature predisposes to ulceration (Armstrong)

-Decreased sweating leads to xerosis and fissuring (portal for infection)

-Abnormal anatomy: extrinsic and intrinsic abnormalities secondary to motor neuropathy and tendon glycosylation.

-Decreased joint mobility: secondary to non-enzymatic glycosylation and excess collagen cross-linking of tendons, ligaments, joint capsules (especially at the STJ and the MTPJ).

-Equinus: Increased cross-linking of collagen in the Achilles tendon (leads to increased forefoot pressures).

-Skin stiffness: secondary to glycosylation of keratin.

-Intrinsic skin weakness: trophic changes associated with PVD.

-All lead to increased plantar pressures, which is the driving force behind ulceration.
-Impaired Wound Healing

-Can be thought of as increased inflammation, decreased vasculature and decreased catabolism.

-Increased Inflammation

-The inflammatory phase of the healing process actually lasts longer than necessary.

-Inflammation initially not as effective due to decreased leukocyte adhesion and morphologic changes to the macrophages.

-Prolongation occurs due to decreased chemotaxis of growth factors and cytokines.

-MMPs increase their activity and continue to produce an “inflammatory soup.”

-All contribute to a wound “stuck” in the inflammatory phase.

-Decreased Vasculature

-Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation.

-Microangiopathy: Thickened basement membrane decreases diffusion at capillary level.

-Mechanism behind neuropathy, nephropathy and retinopathy

-Think of it in terms of a decreased TcPO2

-Endothelial dysfunction:

-Decreased nitric oxide (NO) and prostaglandin to promote vasodilation

-Decreased smooth muscle cell relaxation to promote vasodilation

-AV shunting secondary to autonomic neuropathy

-Decreased vasodilation and membrane permeability in response to trauma/damage/inflammation:

-Usually regulated by substance P and vasomodulators from damaged cells and nociceptors.

-Overall leads to a “sluggish” vasculature with decreased inflow, diffusion, outflow and angiogenesis.

-Decreased Catabolism

-Decreased collagen synthesis, both in peptide production and post-translational modification

-Morphologic changes to keratinocytes

-Decreased angiogenesis

-Shaw JE, Boulton AJ. The pathogenesis of diabetic foot problems: an overview. Diabetes. 1997 Sep; 46 Sep; Suppl 2:S58-61.

-Rathur HM, Boulton AJ. The diabetic foot. Clin Dermatol. 2007 Jan-Feb; 25(1): 109-20.

-Boulton AJ, et al. The global burden of diabetic foot disease. Lancet. 2005 Nov 12; 366(9498): 1719-24.

From: Essential Questions for Surgical Intervention of Diabetic Foot Infections (http://www.podiatrytoday.com/article/8134)

There are different anatomic paradigms that must be considered in terms of the evaluation of the infection source. Certainly depth is one of these paradigms. Absolute depth measurements offer very little clinical information when compared to a functional view of depth from the surgical layers of dissection. An infection should be evaluated in terms of whether it extends through the dermis, superficial fascia, deep fascia, musculotendinous structures or to the level of bone (Table 1). From this general information, specific anatomic structures can then be identified as being within the path of the infection.

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 been used to define the number and boundaries of plantar foot compartments have also given information about relatively consistent fascial clefts where communication between different layers and compartments is likely. These have involved pressurized injection imaging studies where a known compartment is infiltrated with a contrast medium and the extravasation into other compartments can be mapped. The findings of these studies are summarized in Table 2. These communications are obviously numerous and complex. The important concept to realize is that an infection is likely to initially develop within the potential space of a single layer or compartment. There is a tendency for the infection to move proximally or distally before communicating with another layer or compartment. Note however, 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. Intra-operative 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 MPJ level, so distal infections have an increased likelihood of multi-compartment involvement.