HistoryThis section has been translated automatically.
DefinitionThis section has been translated automatically.
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ClassificationThis section has been translated automatically.
- Risk foot, no ulceration, possibly foot deformity
- Superficial ulceration (usually due to improper footwear; see Malum perforans below)
- Foot deformity
- Deep ulcer to the joint capsule, tendons or bones
- Deep ulcer with abscess, osteomyelitis or infection of the joint capsule
- Limited necrosis in the forefoot or heel area
- Necrosis of the entire foot.
Occurrence/EpidemiologyThis section has been translated automatically.
EtiopathogenesisThis section has been translated automatically.
Glycation (non-enzymatic glycosylation) leads to uncontrolled storage of glucose in numerous tissues, e.g. in vessels, nerves, connective tissue, etc..
The consequences are:
- autonomic, motor and sensory nerve disorders (diabetogenic neuropathies)
- Immunosuppression due to glycation of immunocompetent cells (especially macrophages, leukocytes)
- Changes in the flow properties due to an increase in the viscosity of the blood
- Macroangiopahies (carotid artery, large vessels of the legs: PAVK, typically below the knee).
Risk factors for diabetic foot syndrome are:
- Long duration of diabetes:
- High blood glucose levels
- Nicotine abuse
- Presence of retinopathy, nephropathy or neuropathy
- Decreased sensitivity
- Callus formation due to incorrect stress (not painful or only less painful due to neuropathy)
- Reduced muscle strength (limited stabilization of the foot)
- Manifest leg ulcer or ulcer in the anamnesis
- Arterial hypertension
- Lack of exercise
- CVI (chronic venous insufficiency with reduced joint mobility in the ankle joint - arthrogenic congestion syndrome)
- Reduced joint mobility
- Plantar hyperkeratosis
- Unsuitable footwear.
Clinical featuresThis section has been translated automatically.
Initial: Warm, dry, red feet with reduced sensitivity, usually with pronounced callus formation at pressure points.
Progressive: Formation of polyneuropathic, painless ulcers on pressure-exposed areas of the foot (see below Acropathia ulcero-mutilans non-familiaris).
- Infections: mycotic and bacterial infections of varying severity (erysipelas, gram-negative foot infection, foot phlegmon, necrotizing fasciitis, osteomyelitis).
- Charcot arthropathy
- Increasing disease-induced, enforced immobility of patients with its secondary symptoms.
DiagnosisThis section has been translated automatically.
Careful inspection of the feet: neuropathic, non-painful ulcers occurring at pressure points are the typical leading symptom of diabetic foot syndrome
Examination of touch sensitivity
If necessary, radiological diagnostics: DSA or angio-MRI.
TherapyThis section has been translated automatically.
The therapy is based on several pillars:
- Diabetes Optimization
- Pressure relief
- infection control (bacteriological monitoring, also gram-negative germs, e.g. Escherichia coli)
- modern wound management with wound cleansing, if necessary necrosectomy
- Consistent and situation-adapted therapy of the vascular disease.
Wound dressings with silver-activated charcoal overlays are recommended for wound treatment. Later, granulation of the wound can be promoted with a calcium-alginate dressing. Depending on the severity of the damage, minor amputations may be necessary. Education of the patient (wound and diabetes education).
LiteratureThis section has been translated automatically.
- Hertel T et al (2014) Diabetic foot syndrome. Skin14:190-195
- Cracks A (2014) The diabetic foot syndrome. Vasomed 26:191-196
Incoming links (7)Arterial occlusive disease; Arterial occlusive disease peripheral; Diabetic foot; Diabetic foot; Diabetic foot; Hyetellose; Malum perforans;
Outgoing links (4)Acropathia ulcero-mutilans non-familiaris; Arterial occlusive disease peripheral; Charcot arthropathy; Malum perforans;
Please ask your physician for a reliable diagnosis. This website is only meant as a reference.