Steps to prevent diabetic foot ulcers include frequent review by a foot specialist, good foot hygiene, diabetic socks and shoes, as well as avoiding injury.

- Foot-care education combined with increased surveillance can reduce the incidence of serious foot lesions.

Assessment of diabetic foot ulcer includes identifying risk factors such as diabetic peripheral neuropathy, noting that 50 percent of people are asymptomatic, and ruling out other causes of peripheral neuropathy such as alcohol abuse and spinal injury.

The location of the ulcer, its size, shape, depth and whether the tissue is granulating or sloughy needs to be considered. Further considerations include whether the there is malodour, condition of the border of the wound and palpable bone and sinus formation should be investigated. Signs of infection require to be considered such as development of grey or yellow tissue, purulent discharge, unpleasant smell, sinus, undermined edges and exposure of bone or tendon.

Identification of diabetic foot in medical databases, such as commercial claims and prescription data, is complicated by the lack of a specific ICD-9 code for diabetic foot and variation in coding practices. The following codes indicate ulcer of the lower limb or foot:

- 707.1 Ulcer of lower limbs, except pressure ulcer

- 707.14 Ulcer of heel and midfoot

- 707.15 Ulcer of other part of foot

- 707.19 Ulcer of other part of lower limb

One or more codes, in combination with a current or prior diagnosis of diabetes may be sufficient to conclude diabetic foot:

- 250.0 Diabetes Mellitus

- 250.8 Diabetes with other specified manifestations

The lesion can be easily identified clinically. Arterial doppler and pulse volume recordings are performed for baseline assessment of blood flow. Radiographs may be necessary to rule out osteomyelitis.

Prevention of diabetic foot may include optimising metabolic control (regulating glucose levels); identification and screening of people at high risk for diabetic foot ulceration; and patient education in order to promote foot self-examination and foot care knowledge. Patients would be taught routinely to inspect their feet for hyperkeratosis, fungal infection, skin lesions and foot deformities. Control of footwear is also important as repeated trauma from tight shoes can be a triggering factor. There is however only limited evidence that patient education has a long-term impact as a preventative measure.

"Of all methods proposed to prevent diabetic foot ulcers, only foot temperature-guided avoidance therapy was found beneficial in RCTs" according to a meta-analysis.

Diagnosis is clinical. Sensation is tested using graded monofilament.

The prevalence of arterial insufficiency ulcers among people with Diabetes is high due to decreased blood flow caused by the thinning of arteries and the lack of sensation due to diabetic neuropathy. Prevention is the first step in avoiding the development of an arterial insufficiency ulcer. These steps could include annual podiatry check ups that include, "assessment of skin, checking of pedal pulses (assessing for blood flow) and assessing physical sensation".

The management of arterial insufficiency ulcers depends on the severity of the underlying arterial insufficiency. The affected region can sometimes be revascularized via vascular bypass or angioplasty. If infection is present, appropriate antibiotics are prescribed. When proper blood flow is established, debridement is performed. If the wound is plantar (on walking surface of foot), patient is advised to give rest to foot to avoid enlargement of the ulcer. Proper glycemic control in diabetics is important. Smoking should be avoided to aid wound healing.

Treatment of diabetic foot can be challenging and prolonged; it may include orthopaedic appliances, antimicrobial drugs and topical dressings.

Most diabetic foot infections (DFIs) require treatment with systemic antibiotics. The choice of the initial antibiotic treatment depends on several factors such as the severity of the infection, whether the patient has received another antibiotic treatment for it, or whether the infection has been caused by a micro-organism that is known to be resistant to usual antibiotics (e.g. MRSA). The objective of antibiotic therapy is to stop the infection and ensure it does not spread.

It is unclear whether any particular antibiotic is better than any other for curing infection or avoiding amputation. One trial suggested that ertapenem with or without vancomycin is more effective than tigecycline for resolving DFIs. It is also generally unclear whether different antibiotics are associated with more or fewer adverse effects.

It is recommended however that the antibiotics used for treatment of diabetic foot ulcers should be used after deep tissue culture of the wound. Tissue culture and not pus swab culture should be done. Antibiotics should be used at correct doses in order to prevent the emergence of drug resistance.

Underlying cause of neuropathy is first treated. Necrotic portions of the wound are removed and wound is kept moist at associations. Infected ulcers are administered antibiotics.

Skin grafting is one of the options. It has been shown that ultrasound may increase the acceptance of graft at trophic ulcer sites.

In the United Kingdom, the Royal College of Nursing has published guidelines in 'Pressure ulcer risk assessment and prevention' that call for identifying people at risk and taking preventative action; the UK National Standards for Care Homes (UK) to do so as well.

Internationally, the NPUAP, EPUAP and Pan Pacific Pressure Injury Alliance (Australia, New Zealand, Singapore and Hong Kong) published comprehensive evidence-based clinical practice guidelines in 2014. The guideline was developed by an international team of over 100 clinical specialists and updates the 2009 EPUAP and NPUAP clinical guidelines. The guideline includes recommendations on strategies to prevent pressure ulcers including the use of pressure redistributing support surfaces, repositioning and maintaining appropriate nutritional support.

In addition, adequate intake of protein and calories is important. vitamin C has been shown to reduce the risk of pressure ulcers. People with higher intakes of vitamin C have a lower frequency of bed sores in those who are bedridden than those with lower intakes. Maintaining proper nutrition in newborns is also important in preventing pressure ulcers. If unable to maintain proper nutrition through protein and calorie intake, it is advised to use supplements to support the proper nutrition levels. Skin care is also important because damaged skin does not tolerate pressure. However, skin that is damaged by exposure to urine or stool is not considered a pressure ulcer. These skin wounds should be classified as Incontinence Associated Dermatitis.

Some of the investigations done for ulcer are:

- Study of discharging fluid: Culture and sensitivity

- Edge biopsy: Edge contains multiplying cells

- Radiograph of affected area to look for periostitis or osteomyelitis

- FNAC of lymph node

- Chest X-ray and Mantoux test in suspected tuberculous ulcer

Compression stockings appear to prevent the formation of new ulcers in people with a history of venous ulcers.

Patients with diabetes and proximal (hip, thigh) pain and weakness are often suspected of having diabetic amyotrophy. More definitive diagnosis is commonly made with electrodiagnostic studies including nerve conduction studies (NCS) and electromyogram (EMG). Diabetic amyotrophy is often a diagnosis of exclusion in diabetic patients with a lumbosacral plexopathy for whom no other cause of lumbosacral plexopathy can be determined.

The main aim of the treatment is to create such an environment that allows skin to grow across an ulcer. In the majority of cases this requires finding and treating underlying venous reflux and National Institute for Health and Care Excellence (NICE) recommends referral to a vascular service for anyone with a leg ulcer that has not healed within 2 weeks or anyone with a healed leg ulcer.

Most venous ulcers respond to patient education, elevation of foot, elastic compression and evaluation, called the Bisgaard regimen. There is no evidence for intravenous or by mouth antibiotics for venous leg ulcers. Silver products are also not typically useful while there is some evidence for cadexomer iodine creams. There is a lack of quality evidence regarding the use of medical grade honey for venous leg ulcers.

Tissue biopsy is the gold standard. Macroscopically this reveals pale muscle tissue. Microscopically infarcted patches of myocytes. Necrotic muscle fibers are swollen and eosinophilic and lack striations and nuclei. Small-vessel walls are thickened and hyalinized, with luminal narrowing or complete occlusion. Biopsy cultures for bacteria, fungi, acid-fast bacilli and stains are negative in simple myonecrosis.

Creatine kinase may be normal or increased probably depending upon the stage of the condition when sampling is undertaken. ESR is elevated. Planar X-ray reveals soft tissue swelling and may potentially show gas within necrotic muscle, Bone scan may show non specific uptake later in the course. CT shows muscle oedema with preserved tissue planes (non-contrast enhancing). MRI is the exam of choice and shows increased signal on T2 weighted images within areas of muscle oedema. Contrast enhancement is helpful but must be weighed against the risk of Nephrogenic Systemic Fibrosis as many diabetics have underlying renal insufficiency. Arteriography reveals large and medium vessel arteriosclerosis occasionally with dye within the area of tissue infarction . Electromyography shows non specific focal changes.

Skin ulcers may take a very long time to heal. Treatment is typically to avoid the ulcer getting infected, remove any excess discharge, maintain a moist wound environment, control the edema, and ease pain caused by nerve and tissue damage.

Topical antibiotics are normally used to prevent the ulcer getting infected, and the wound or ulcer is usually kept clear of dead tissue through surgical debridement.

Commonly, as a part of the treatment, patients are advised to change their lifestyle if possible and to change their diet. Improving the circulation is important in treating skin ulcers, and patients are consequently usually recommended to exercise, stop smoking, and lose weight.

In recent years, advances have been made in accelerating healing of chronic wounds and ulcers. Chronic wounds produce fewer growth hormones than necessary for healing tissue, and healing may be accelerated by replacing or stimulating growth factors while controlling the formation of other substances that work against them.

Leg ulcers can be prevented by using compression stockings to prevent blood pooling and back flow. It is likely that a person who has had a skin ulcer will have it again; use of compression stockings every day for at least 5 years after the skin ulcer has healed may help to prevent recurrence.

Diabetic peripheral neuropathy is the most likely diagnosis for someone with diabetes who has pain in a leg or foot, although it may also be caused by vitamin B deficiency or osteoarthritis. A 2010 review in the Journal of the American Medical Association's "Rational Clinical Examination Series" evaluated the usefulness of the clinical examination in diagnosing diabetic peripheral neuropathy. While the physician typically assesses the appearance of the feet, presence of ulceration, and ankle reflexes, the most useful physical examination findings for large fiber neuropathy are an abnormally decreased vibration perception to a 128-Hz tuning fork (likelihood ratio (LR) range, 16–35) or pressure sensation with a 5.07 Semmes-Weinstein monofilament (LR range, 11–16). Normal results on vibration testing (LR range, 0.33–0.51) or monofilament (LR range, 0.09–0.54) make large fiber peripheral neuropathy from diabetes less likely. Combinations of signs do not perform better than these 2 individual findings. Nerve conduction tests may show reduced functioning of the peripheral nerves, but seldom correlate with the severity of diabetic peripheral neuropathy and are not appropriate as routine tests for the condition.

Diagnosis is mostly based on the clinical appearance and the medical history. The most important diagnostic feature is a history of recurrent, self healing ulcers at fairly regular intervals. Although there are many causes of oral ulceration, "recurrent" oral ulceration has relatively few causes, most commonly aphthous stomatitis, but rarely Behçet's disease, erythema multiforme, ulceration associated with gastrointestinal disease, and recurrent intra-oral herpes simplex infection. A systemic cause is more likely in adults who suddenly develop recurrent oral ulceration with no prior history.

Special investigations may be indicated to rule out other causes of oral ulceration. These include blood tests to exclude anemia, deficiencies of iron, folate or vitamin B12 or celiac disease. However, the nutritional deficiencies may be latent and the peripheral blood picture may appear relatively normal. Some suggest that screening for celiac disease should form part of the routine work up for individuals complaining of recurrent oral ulceration. Many of the systemic diseases cause other symptoms apart from oral ulceration, which is in contrast to aphthous stomatitis where there is isolated oral ulceration. Patch testing may be indicated if allergies are suspected (e.g. a strong relationship between certain foods and episodes of ulceration). Several drugs can cause oral ulceration (e.g. nicorandil), and a trial substitution to an alternative drug may highlight a causal relationship.

Tissue biopsy is not usually required, unless to rule out other suspected conditions such as oral squamous cell carcinoma. The histopathologic appearance is not pathognomonic (the microscopic appearance is not specific to the condition). Early lesions have a central zone of ulceration covered by a fibrinous membrane. In the connective tissue deep to the ulcer there is increased vascularity and a mixed inflammatory infiltrate composed of lymphocytes, histiocytes and polymorphonuclear leukocytes. The epithelium on the margins of the ulcer shows spongiosis and there are many mononuclear cells in the basal third. There are also lymphocytes and histiocytes in the connective tissue surrounding deeper blood vessels near to the ulcer, described histologically as "perivascular cuffing".

Proper management of diabetes mellitus can prevent proximal diabetic neuropathy from ever occurring.

The incidence of proximal diabetic neuropathy incidence is thought to be correlated to blood glucose control in diabetics, and is likely reversible with better control.

Medication helps reduce the pain involved in proximal diabetic neuropathy. Most patients take oral medication that is prescribed by a doctor. Common types of medication used to treat diabetic amyotrophy include anticonvulsives (e.g. gabapentin, pregabalin) as well as opioid medications, although the latter category is not optimally indicated for neuropathic pain.

Soft tissue constriction on the medial aspect of the fifth toe is the most frequently presented radiological sign in the early stages. Distal swelling of the toe is considered to be a feature of the disease. In grade III lesions osteolysis is seen in the region of the proximal interphalangeal joint with a characteristic tapering effect. Dispersal of the head of the proximal phalanx is frequently seen. Finally, after autoamputation, the base of the proximal phalanx remains. Radiological examination allows early diagnosis and staging of ainhum. Early diagnosis is crucial to prevent amputation.

Doppler shows decreased blood flow in posterior tibial artery.

Ainhum is an acquired and progressive condition, and thus differs from congenital annular constrictions. Ainhum has been much confused with similar constrictions caused by other diseases such as leprosy, diabetic gangrene, syringomyelia, scleroderma or Vohwinkel syndrome. In this case, it is called pseudo-ainhum, treatable with minor surgery or intralesional corticosteroids, as with ainhum. It has even been seen in psoriasis or it is acquired by the wrapping toes, penis or nipple with hairs, threads or fibers. Oral retinoids, such as tretinoin, and antifibrotic agents like tranilast have been tested for pseudo-ainhum. Impending amputation in Vohwinkel syndrome can sometimes be aborted by therapy with oral etretinate. It is rarely seen in the United States but often discussed in the international medical literature.

Diagnosis is made by clinical observation and the following tests.

(1) Gram stain of the fluid from pustules or bullae, and tissue swab.

(2) Blood culture

(3) Urine culture

(4) Skin biopsy

(5) Tissue culture

Magnetic resonance imaging can be done in case of ecthyma gangrenosum of plantar foot to differentiate from necrotizing fasciitis.

Outcomes vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair was necessary. Average healing times vary from 55–97 days depending on location. Up to 1–2 years may be required for complete healing.

Adequate footwear is important to prevent trauma. General good health and nutrition also reduce ulcer risk. Adequate and prompt cleansing and treatment of ankle and leg skin breaks is also important. Improving hygiene and nutrition may help to prevent tropical ulcers.

Corns and calluses are easier to prevent than to treat. When it is usually not desirable to form a callus, minimizing rubbing and pressure will prevent callus formation. Footwear should be properly fitted, gloves may be worn, and protective pads, rings or skin dressings may be used. People with poor circulation or sensation should check their skin often for signs of rubbing and irritation so they can minimize any damage.