The document summarizes guidelines from the International Working Group on the Diabetic Foot (IWGDF) for the prevention and management of diabetic foot disease. It provides an overview of updates to the 2019 guidelines, including new recommendations and reordering of ulcer treatment principles. Key aspects of diabetic foot disease and ulcer assessment, classification, and treatment are described, including risk factors, offloading, wound care, infection treatment, and revascularization. Guidelines for active Charcot neuro-osteoarthropathy are also summarized.

1. 2 0 1 9 & 2 0 2 3

2. Introduction
IWGDF Practical Guidelines describe the basic
principles of prevention and management of
diabetic foot disease.

3. Evidence-based IWGDF Guidelines (2023 update):
• Prevention of foot ulcers in persons with diabetes (1)
• Classification of diabetes-related foot ulcers (2)
• Diagnosis and treatment of foot infection in persons with diabetes (3)
• Diagnosis and management of peripheral artery disease in persons with a foot
ulcer and diabetes (4)
• Offloading foot ulcers in persons with diabetes (5)
• Interventions to enhance healing of foot ulcers in persons with diabetes (6)
• Acute Charcot neuro-osteoarthropathy (7)

4. IWGDF Guidelines (2023 update):
Compared to the previous version of these practical
guidelines (the 2019 update: (21)), the following is new in
this 2023 update: several new recommendations in various
sections based on the updated guidelines, re-ordering of the
ulcer treatment principles, based on the order for clinical
decision-making, and a summary of the IWGDF guidelines on
the diagnosis and management of acute Charcot’s neuro-
osteoarthropathy.

5. Diabetic Foot Disease
• Diabetic Foot Disease is among the most serious
complications of diabetes mellitus
• It is a source of major suffering and financial cost for the
patient, also a considerable burden on the patients family,
healthcare professionals and facilities and society in general
• Strategies includes: prevention, patient and staff
education, multidisciplinary treatment, and close
monitoring

6. Patophysiology
• The pathway to ulceration are similar in most patients.
• These ulcers frequently results from a person with diabetes
simultaneously having two or more risk factors, with
diabetic peripheral neuropathy and peripheral artery
disease (PAD)

7. Neuropathy
•The neuropathy  leads to insensitive and
sometimes deformed foot.
•In neuropathy, minor trauma can precipitate
ulceration of the foot (e.g: ill-fitting shoes or an acute
mechanical or thermal injury)

8. Loss of protective sensation, foot deformities, and limited joint
mobility can result in abnormal biomechanical loading of the foot. This
produces high mechanical stress in some areas, the response to which
is usually thickened skin (callus). The callus then leads to a further
increase in the loading of the foot, often with subcutaneous
haemorrhage and eventually skin ulceration.

9. Peripheral Artery Disease (PAD)
• PAD generally caused by atherosclerosis, is present in up to 50% of
patients with a diabetic foot ulcer.
• A small percentage of foot ulcers in patients with severe PAD are
purely ischaemic; these are usually painful and may follow minor
trauma
• The majority of foot ulcers, however, are either purely neuropathic
or neuro-ischaemic, i.e., caused by combined neuropathy and
ischaemia

10. FOOT ULCER PREVENTION
There are five key elements to prevent foot ulcers:
1.Identify the person with an at-risk foot
2.Regularly inspect and examine the feet of a person at-risk for foot
ulceration
3.Provide structured education for patients, their family and
healthcare professionals
4.Encourage routine wearing of appropriate footwear
5.Treat risk factors for ulceration

11. Areas of the foot at highest risk for ulceration

12. Footwear should be sufficiently wide
to accommodate the foot without
excessive pressure on the skin
The proper way to cut toe nails

13. ASSESSMENT & TREATMENT
OF FOOT ULCERS

14. ASSESSMENT OF FOOT ULCERS
Classification of the foot ulcer: the foot ulcer should be classified
following the assessment of the six items of the SINBAD system.
1. “SITE”: Describe where the ulcer is located on the foot. This
includes description of forefoot, midfoot or hindfoot, but it is
also suggested to differentiate between plantar, interdigital,
medial, lateral or dorsal.

15. ASSESSMENT OF FOOT ULCERS
2. “ISCHEMIA”: Assess if pedal blood flow is intact (at least one
palpable pulse), or if there is clinical evidence of reduced blood flow.
Further, examine the arterial pedal wave forms (with a Doppler
instrument), measure the ankle and toe pressures, and calculate the
ankle-brachial index (ABI) and toe-brachial index (TBI).

16. ASSESSMENT OF FOOT ULCERS
3. “Neuropathy”: Assess if protective sensation is intact or
lost  DOING A SENSORY FOOT EXAMINATION

17. ASSESSMENT OF FOOT ULCERS
4. “Bacterial infection”: Assess if clinical infection is present.
Diagnose infection by the presence of at least two clinical
signs or symptoms of inflammation (redness, warmth,
induration, pain/tenderness) or purulent secretions.
Infections should be classified using the IWGDF/IDSA grading as mild
(superficial ulcer with minimal cellulitis), moderate (ulcer deeper than
skin or more extensive cellulitis, with or without abcess) or severe
(accompanied by systemic signs of sepsis), with or without
osteomyelitis.

18. ASSESSMENT OF FOOT ULCERS
5. “Area”: Measure ulcer area and express in cm2.
6. “Depth”: Assess ulcer depth and classify as: confined
to skin and subcutaneous tissue; reaching muscle or
tendon; or reaching bone. Determining depth can be
difficult, especially in the presence of overlying callus or
necrotic tissue.

19. CLASSIFICATION AND TYPE
•IWGDF/ISDA  assess the severity of infection
•WIfI (wound/ischaemia/infection) system  In
patients with PAD (to stratify amputation risk and
revascularisation benefit)
•SINBAD system  For communication among
healthcare professionals, also be used for audit of
outcome of populations

20. Principles of Ulcer Treatment
1. Treatment of infection
2. Restoration of tissue perfusion
3. Pressure offloading and ulcer protection
4. Local ulcer care
5. Person Centered Care
6. Education for patient and relatives

21. 1. Treatment of Infection
• Superficial ulcer with limited soft tissue (mild) infection:
• Cleanse, debride all necrotic tissue and surrounding callus
• Start empiric oral antibiotic therapy targeted at Staphylococcus aureus and
streptococci (unless there are reasons to consider other, or additional, likely
pathogens)

22. • Deep or extensive (potentially limb-threatening) infection (moderate
or severe infection):
• Urgently evaluate for need for surgical intervention to remove necrotic tissue,
including infected
• bone, release compartment pressure or drain abscesses
• Assess for PAD; if present consider urgent treatment, including
revascularization
• Initiate empiric, parenteral, broad-spectrum antibiotic therapy, aimed at
common gram-positive and gram-negative bacteria, including obligate
anaerobes
• Adjust (constrain and target, if possible) the antibiotic regimen based on both
the clinical response to empirical therapy and culture and sensitivity results

23. 2. Restoration of Tissue Perfusion
• Revascularization if:
• An ankle pressure <50mm Hg or an ABI <0.5  consider urgent vascular imaging
• A toe pressure is <30mmHg or TcpO2 is <25 mmHg
• When an ulcer fails to show signs of healing within 6 weeks, despite optimal management
• The aim of revascularization:
• to restore direct flow to at least one of the foot arteries, preferably the artery that supplies
the anatomical region of the wound
• Select a revascularization technique based on both individual factors (the patients
factor and the local operator expertise

24. • After a revascularization procedure  effectiveness should be
evaluated with an objective measurement of perfusion
• Pharmacological treatments to improve perfusion have not been
proven to be beneficial
• Emphasise efforts to reduce cardiovascular risk (cessation of smoking,
control of hypertension and dyslipidaemia, use of anti-platelet drugs)

25. • Non-removable knee-high offloading device
• a total contact cast (TCC)
• Removable knee-high offloading device
• Ankle-high offloading device
• If biomechanical relief are not available  using felted foam, but only
in combination with appropriate footwear
3. Pressure offloading and ulcer protection

26. 4. Local Ulcer Care
• Regular inspection of the ulcer by a trained health care provider is
essential
• Debride the ulcer and remove surrounding callus (preferably with
sharp surgical instruments), and repeat as needed
• Select dressings to control excess exudation and maintain moist
environment
• Do not soak the feet, as this may induce skin maceration.
• Consider negative pressure to help heal post-operative wounds

27. Consider one of the following adjunctive treatments in non-infected
ulcers that fail to heal after 4-6 weeks despite optimal clinical care:
• A sucrose octasulfate impregnated dressing in neuro-ischemic ulcers (without
severe ischemia)
• A multi-layered patch of autologous leucocytes, platelets and fibrin in ulcers
with or without moderate ischemia
• Placental membrane allografts in ulcers with or without moderate ischemia
• Systemic oxygen therapy as an adjunctive treatment in ischaemic ulcers that
do not heal despite revascularisation

28. • The following treatments are not well-supported for routine ulcer
management:
• Biologically active products (collagen, growth factors, bio- engineered tissue)
in neuropathic ulcers
• Silver, or other antimicrobial agent, containing dressings or topical
applications

29. 5. Person Centered Care
• Optimise glycaemic control, if necessary, with insulin.
• Treat oedema or malnutrition, if present.
• Treat cardiovascular risk factors.
• Treat depression or other psycho-social difficulties.

30. 6. Education for Patients and Relatives
• Instruct patients (and relatives or carers) on appropriate foot ulcer
self-care and how to recognize and report signs and symptoms of new
or worsening infection (e.g., onset of fever, changes in local wound
conditions, worsening hyperglycaemia)
• During a period of enforced bed rest, instruct on how to prevent an
ulcer on the contra- lateral foot

31. ACTIVE CHARCOT NEURO-OSTEOARTHROPATHY (CNO)
• In any person with diabetes mellitus and with a red, hot, swollen foot, the diagnosis of active
CNO should be considered. As described in our Charcot guidelines, CNO is a sterile inflammatory
process in persons with neuropathy that results in injury to bones, joints and soft tissues
• The diagnosis is based on the aforementioned clinical findings of inflammation after
exclusion of other causes and abnormalities on imaging. If these abnormalities are not
seen on plain X-ray, an MRI should be performed; if an MRI is not possible, perform a
CT-scan and/or a radionucleotide scan. When such advanced imaging is not possible the
person should be treated as having a probable active CNO.
• If not treated adequately, it can result in progressive fracturing and dislocations resulting
in a deformed foot
• The diagnosis is based on the aforementioned clinical findings of inflammation after
exclusion of other causes and abnormalities on imaging. If these abnormalities are not
seen on plain X-ray, an MRI should be performed; if an MRI is not possible, perform a
CT-scan and/or a radionucleotide scan

32. ACTIVE CHARCOT NEURO-OSTEOARTHROPATHY (CNO)
• In order to promote remission of the disease and to prevent (progressive)
deformity, the affected extremity should be offloaded and immobilized.
• Treatment should start once the diagnosis is considered and continue
until clinical remission with consolidation of fractures is achieved. As long
as there are clinical signs of inflammation the offloading should be
continued.
• Currently there is no medical therapy that can shorten the duration of
disease or prevent deformities, such interventions are therefore not
recommended. Vitamin D and calcium should be supplemented
according to local guidelines for persons with an elevated risk of
inadequate vitamin D levels.
• The knee-high cast can be stopped when there are no clinical signs of
inflammation with radiographic consolidation of fractures (if present) on
plain X-ray.

33. THANK YOU