**1.3 Trauma and infection**

Trauma might also contribute to the development of ulceration in DFU. Ill-fitting shoes are the most prevalent source of trauma, and also injuries go missed due to a lack of sensation [14]. Motor neuropathy causes structural changes in the structure of the foot; as a result, many regular shoes are inappropriate for diabetic patients. Walking-related repetitive stress, along with diminished sensation and proprioception, predisposes to skin damage by producing atrophy and displacement of protective plantar fat pads, leading to ulceration and infection with inadequate skin protection or inappropriate footwear [15].

Neglecting skin protection, such as forgetting to apply moisturising lotions or failing to recognise cutaneous stress (redness, blister formation), can lead to ulceration

**Figure 1.** *Common pathway to diabetic foot ulcer.*

and the development of an invasive soft-tissue infection. If not treated quickly, tissue degradation will persist, especially if the patient continues to walk. The risk of ulceration increases significantly in the presence of peripheral neuropathy, foot deformity or previous digit amputation (by 32 times) [1].

Trauma in the foot could also lead into infection that penetrates the deep fascia, allowing infection to spread into the mid-foot muscles, joints and tendon sheaths. In diabetics, infection is responsible for 50% of all major (above- or below-knee) lower-extremity amputations. Polymicrobial infections (staphylococci, streptococci, enterococci, Escherichia coli and other Gram-negative bacteria) are widespread, as is the presence of antibiotic-resistant bacterial strains, particularly methicillin-resistant Staphylococcus aureus, which occurs in 30–40% of cases. When a diabetic foot infection contains resistant bacterial strains, which is commonly the result of repeated or protracted antibiotic use, the risk of amputation rises [16]. The common pathway to DFU is illustrated in **Figure 1**.
