Diabetic foot ulcers: A devastating complication of diabetes mellitus continues non-stop in spite of new medical treatment modalities

Table 1 Wagner-Meggit classification

Grade	Lesion
0	No open lesion
1	Superficial ulcer
2	Deep ulcer to tendon or joint capsule
3	Deep ulcer with abscess, osteomyelitis or joint sepsis
4	Local gangrene - fore foot or heel
5	Gangrene of entire foot

Table 2 University of Texas Classification system

	0	1	2	3
A	No open lesion	Superficial wound	Affected tendon/capsules	Affected bone/joint
B	With infection	With infection	With infection	With infection
C	Ischemic	Ischemic	Ischemic	Ischemic
D	Infection/ischemia	Infection/ischemia	Infection/ischemia	Infection/ischemia

Table 3 Wound, Ischemia, and foot Infection classification

	Wound	Ischemia; toe pressure/tcpo2	Infection
0	No ulcer and no gangrene	> 60 mm/Hg	Non-infected
1	Small ulcer and no gangrene	40-59 mm/Hg	Mild (< 2 cm sellulitis)
2	Deep ulcer and gangrene limited to toes	30-39 mm/Hg	Moderate (> 2 cm sellulitis)
3	Extensive ulcer or extensive gangrene	< 30 mm/Hg	Severe (systemic response/sepsis)

Table 4 Standard care of diabetic foot ulcer

Treatment	Description
Debridement	Surgical debridement	Necrotic or non-viable tissue should be removed, regular (weekly) debridement is associated with rapid healing of ulcers
Dressing	Films, foams, hydrocolloids, hydrogel	Proper using of dressing materials could facilitate moist environment
Wound off-loading	Rock or bottom outsoles, custom-made insoles, some shoe inserts	Plantar shear stress should be removed
Vascular assessment	PTA or endovascular recanalization followed by PTA or by-pass grafting	Arterial insufficiency should be treated for improving wound healing
Control of infection	Appropriate antibiotic therapy according to pathogens	Deep tissue cultures should be obtained before antibiotic therapy, for mild infection treatment duration could be 1-2 wk but for moderate to severe infection, it should be 3-4 wk
Glycemic control		For better glycemic control, insulin treatment has been preferred in hospitalized patients with diabetic foot ulcers

PTA: Percutaneous transluminal angioplasty.

Table 5 Additional adjuvant care of diabetic foot ulcer

Item	Description
Negative pressure wound therapy (VAC)	Widely used, removal of the excess third space fluid from the area, reduction of bacterial load, increased granulation tissue, but RCTs have high risk of bias
Synthetic skin grafts (Bio-engineered skin substitutes)	Contribute to the new dermal tissue but limited data to prove benefit of these products
Non-surgical debridement agents (enzymatic debridement, autolytic debridement, hydroterapy, Maggot therapy)	Promoting fibroblast migration and improving skin perfusion but due to small RCTs, it has clinical bias for beneficial effect
Topical growth factors (EGF, VEGF, PDGF, FGF)	Promote healing non-infected foot ulcer and stimulating angiogenesis but limited trials confirming positive outcomes
Electrical stimulation	Bacteriostatic and bactericidal effect on foot ulcer but lack of evidence due to limited clinical trials
HBOC	HBOC therapy increases blood and oxygen content in hypoxic tissues and has antimicrobial activity, but it is unclear whether it has benefit in long term wound healing

RCT: Randomised controlled studies; HBOC: Hyperbaric oxygen chambers; VAC: Vacuum assisted closure; EGF: Epidermal growth factor; VEGF: Vascular endotelial growth factor; PDGF: Platelet derived growth factor; FGF: Fibroblast growth factor.