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.

There are many types of dressings used to treat diabetic foot ulcers such as absorptive fillers, hydrogel dressings, and hydrocolloids. There is no good evidence that one type of dressing is better than another for diabetic foot ulcers. In selecting dressings for chronic non healing wounds it is recommended that the cost of the product be taken into account.

Hydrogel dressings may have shown a slight advantage over standard dressings, but the quality of the research is of concern. Dressings and creams containing silver have not been properly studied nor have alginate dressings. Biologically active bandages that combine hydrogel and hydrocolloid traits are available, however more research needs to be conducted as to the efficacy of this option over others.

The length of antibiotic courses depend on the severity of the infection and whether bone infection is involved but can range from 1 week to 6 weeks or more. Current recommendations are that antibiotics are only used when there is evidence of infection and continued until there is evidence that the infection has cleared, instead of evidence of ulcer healing. Choice of antibiotic depends on common local bacterial strains known to infect ulcers. Microbiological swabs are believed to be of limited value in identifying causative strain. Microbiological investigation is of value in cases of osteomyelitis. Most ulcer infections involve multiple microorganisms.

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.

Typical opioid medications, such as oxycodone, appear to be no more effective than placebo. In contrast, low-quality evidence supports a moderate benefit from the use of atypical opioids (e.g., tramadol and tapentadol), which also have SNRI properties. Opioid medications are recommended as second or third-line treatment for DPN.

TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line treatment for DPN. Of the TCAs, imipramine has been the best studied. These medications are effective at decreasing painful symptoms but suffer from multiple side effects that are dose-dependent. One notable side effect is cardiac toxicity, which can lead to fatal abnormal heart rhythms. Additional common side effects include dry mouth, difficulty sleeping, and sedation. At low dosages used for neuropathy, toxicity is rare, but if symptoms warrant higher doses, complications are more common. Among the TCAs, amitriptyline is most widely used for this condition, but desipramine and nortriptyline have fewer side effects.

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.

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.

These ulcers are difficult to heal by basic wound care and require advanced therapy, such as hyperbaric oxygen therapy or bioengineered skin substitutes. If not taken care of in time, there are very high chances that these may become infected and eventually may have to be amputated. Individuals with history of previous ulcerations are 36 times more likely to develop another ulcer.

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.

In some cases, a pancreas transplant can restore proper glucose regulation. However, the surgery and accompanying immunosuppression required may be more dangerous than continued insulin replacement therapy, so is generally only used with or some time after a kidney transplant. One reason for this is that introducing a new kidney requires taking immunosuppressive drugs such as cyclosporine, which allows the introduction of a new pancreas to a person with diabetes without any additional immunosuppressive therapy. However, pancreas transplants alone may be beneficial in people with extremely labile type 1 diabetes mellitus.

Injections of insulin—either via subcutaneous injection or insulin pump— are necessary for those living with type 1 diabetes because it cannot be treated by diet and exercise alone. Insulin dosage is adjusted taking into account food intake, blood glucose levels and physical activity.

Untreated type 1 diabetes can commonly lead to diabetic ketoacidosis which is a diabetic coma which can be fatal if untreated. Diabetic ketoacidosis can cause cerebral edema (accumulation of liquid in the brain). This is a life-threatening issue and children are at a higher risk for cerebral edema than adults, causing ketoacidosis to be the most common cause of death in pediatric diabetes.

Treatment of diabetes focuses on lowering blood sugar or glucose (BG) to the near normal range, approximately 80–140 mg/dl (4.4–7.8 mmol/L). The ultimate goal of normalizing BG is to avoid long-term complications that affect the nervous system (e.g. peripheral neuropathy leading to pain and/or loss of feeling in the extremities), and the cardiovascular system (e.g. heart attacks, vision loss). This level of control over a prolonged period of time can be varied by a target HbA level of less than 7.5%.

There are four main types of insulin: rapid acting insulin, short-acting insulin, intermediate-acting insulin, and long-acting insulin. The rapid acting insulin is used as a bolus dosage. The action onsets in 15 minutes with peak actions in 30 to 90 minutes. Short acting insulin action onsets within 30 minutes with the peak action around 2 to 4 hours. Intermediate acting insulin action onsets within one to two hours with peak action of four to 10 hours. Long-acting insulin is usually given once per day. The action onset is roughly 1 to 2 hours with a sustained action of up to 24 hours. Some insulins are biosynthetic products produced using genetic recombination techniques; formerly, cattle or pig insulins were used, and even sometimes insulin from fish.

People with type 1 diabetes always need to use insulin, but treatment can lead to low BG (hypoglycemia), i.e. BG less than 70 mg/dl (3.9 mmol/l). Hypoglycemia is a very common occurrence in people with diabetes, usually the result of a mismatch in the balance among insulin, food and physical activity. Symptoms include excess sweating, excessive hunger, fainting, fatigue, lightheadedness and shakiness. Mild cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and are treated with intravenous glucose or injections with glucagon. Continuous glucose monitors can alert patients to the presence of dangerously high or low blood sugar levels, but technical issues have limited the effect these devices have had on clinical practice.

As of 2016 an artificial pancreas looks promising with safety issues still being studied.

The mainstay of treatment, like the treatment of gangrene, is surgical debridement, and often includes amputation.

Medications used to treat diabetes do so by lowering blood sugar levels. There are a number of different classes of anti-diabetic medications. Some are available by mouth, such as metformin, while others are only available by injection such as GLP-1 agonists. Type 1 diabetes can only be treated with insulin, typically with a combination of regular and NPH insulin, or synthetic insulin analogs.

Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose. Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin. When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications. Doses of insulin are then increased to effect.

Since cardiovascular disease is a serious complication associated with diabetes, some have recommended blood pressure levels below 130/80 mmHg. However, evidence supports less than or equal to somewhere between 140/90 mmHg to 160/100 mmHg; the only additional benefit found for blood pressure targets beneath this range was an isolated decrease in stroke risk, and this was accompanied by an increased risk of other serious adverse events. A 2016 review found potential harm to treating lower than 140 mmHg. Among medications that lower blood pressure, angiotensin converting enzyme inhibitors (ACEIs) improve outcomes in those with DM while the similar medications angiotensin receptor blockers (ARBs) do not. Aspirin is also recommended for people with cardiovascular problems, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.

Oral medications like Glipizide that stimulate the pancreas, promoting insulin release (or in some cases, reduce glucose production), are less and less used in cats, and these drugs may be completely ineffective if the pancreas is not working. These drugs have also been shown in some studies to damage the pancreas further or to cause liver damage. Some owners are reluctant to switch from pills to insulin injections, but the fear is unjustified; the difference in cost and convenience is minor (most cats are easier to inject than to pill), and injections are more effective at treating the disease.

An acute hypoglycemic episode (very low blood sugar) can happen to even careful pet owners, since cats' insulin requirements sometimes change without warning. The symptoms include depression/lethargy, confusion/dizziness, loss of excretory/bladder control, vomiting, and then loss of consciousness and/or seizures. Immediate treatment includes administering honey or corn syrup by rubbing on the gums of the cat (even if unconscious, but not if in seizures). Symptomatic hypoglycemia in cats is a medical emergency and the cat will require professional medical attention. The honey/corn syrup should continue to be administered on the way to the vet, as every minute without blood sugar causes brain damage.

A cat with hypoglycemia according to a blood glucose meter (<2.2 mmol/L or 40 mg/dL), but with no symptoms, should be fed as soon as possible. Hypoglycemic cats that refuse to eat can be force-fed honey or corn syrup until they stabilize.

Mild hypoglycemic episodes can go unnoticed, or leave evidence such as urine pools outside the litter box. In these cases the blood sugar will probably appear paradoxically "high" upon the next test hours later, since the cat's body will react to the low blood sugar by stimulating the liver to release stored glycogen.

People with diabetes can benefit from education about the disease and treatment, good nutrition to achieve a normal body weight, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.

There is no single dietary pattern that is best for all people with diabetes. For overweight people with type 2 diabetes, any diet that the person will adhere to and achieve weight loss on is effective.

Treatment includes supportive care with analgesics and anti-inflammatory agents. Exercise should be limited as it increases pain and extends the area of infarction. Symptoms usually resolve in weeks to months, but fifty percent of sufferers will experience relapse in either leg.

In some cases, foot diseases and painful conditions can be treated. Synovium hydrates the cartilage in the heal and can bring pain relief quickly. Synovium gel looks as well as strongly smells like urine, straying some consumers away. However this only occurs after expiration. Blood thinners can also work however are deemed as bad relievers by medical practitioners due to the fact that they can contribute to headaches and in some cases increase foot pain afterwards.

Trench foot can be prevented by keeping the feet clean, warm, and dry. It was also discovered in World War I that a key preventive measure was regular foot inspections; soldiers would be paired and each made responsible for the feet of the other, and they would generally apply whale oil to prevent trench foot. If left to their own devices, soldiers might neglect to take off their own boots and socks to dry their feet each day, but if it were the responsibility of another, this became less likely. Later on in the war, instances of trench foot began to decrease, probably as a result of the introduction of the aforementioned measures; of wooden duckboards to cover the muddy, wet, cold ground of the trenches; and of the increased practice of troop rotation, which kept soldiers from prolonged time at the front.

Cerebral edema, if associated with coma, often necessitates admission to intensive care, artificial ventilation, and close observation. The administration of fluids is slowed. The ideal treatment of cerebral edema in DKA is not established, but intravenous mannitol and hypertonic saline (3%) are used—as in some other forms of cerebral edema—in an attempt to reduce the swelling.

The administration of sodium bicarbonate solution to rapidly improve the acid levels in the blood is controversial. There is little evidence that it improves outcomes beyond standard therapy, and indeed some evidence that while it may improve the acidity of the blood, it may actually worsen acidity inside the body's cells and increase the risk of certain complications. Its use is therefore discouraged, although some guidelines recommend it for extreme acidosis (pH<6.9), and smaller amounts for severe acidosis (pH 6.9–7.0).

Modulating and ameliorating diabetic complications may improve the overall quality of life for diabetic patients. For example; when elevated blood pressure was tightly controlled, diabetic related deaths were reduced by 32% compared to those with less controlled blood pressure.

There are many topical antifungal drugs useful in the treatment of athlete's foot including: miconazole nitrate, clotrimazole, tolnaftate (a synthetic thiocarbamate), terbinafine hydrochloride, butenafine hydrochloride and undecylenic acid. The fungal infection may be treated with topical antifungal agents, which can take the form of a spray, powder, cream, or gel. Topical application of an antifungal cream such as terbinafine once daily for one week or butenafine once daily for two weeks is effective in most cases of athlete's foot and is more effective than application of miconazole or clotrimazole. Plantar-type athlete's foot is more resistant to topical treatments due to the presence of thickened hyperkeratotic skin on the sole of the foot. Keratolytic and humectant medications such as urea, salicyclic acid (Whitfield's ointment), and lactic acid are useful adjunct medications and improve penetration of antifungal agents into the thickened skin. Topical glucocorticoids are sometimes prescribed to alleviate inflammation and itching associated with the infection.

A solution of 1% potassium permanganate dissolved in hot water is an alternative to antifungal drugs. Potassium permanganate is a salt and a strong oxidizing agent.

Once the process is recognized, it should be treated via the VIPs — vascular management, infection management and prevention, and pressure relief. Aggressively pursuing these three strategies will progress the healing trajectory of the wound. Pressure relief (off-loading) and immobilization with total contact casting (TCC) are critical to helping ward off further joint destruction.

TCC involves encasing the patient’s complete foot, including toes, and the lower leg in a specialist cast that redistributes weight and pressure in the lower leg and foot during everyday movements. This redistributes pressure from the foot into the leg, which is more able to bear weight, to protect the wound, letting it regenerate tissue and heal. TCC also keeps the ankle from rotating during walking, which prevents shearing and twisting forces that can further damage the wound. TCC aids maintenance of quality of life by helping patients to remain mobile.

There are two scenarios in which the use of TCC is appropriate for managing neuropathic arthropathy (Charcot foot), according to the American Orthopaedic Foot and Ankle Society. First, during the initial treatment, when the breakdown is occurring, and the foot is exhibiting edema and erythema; the patient should not bear weight on the foot, and TCC can be used to control and support the foot. Second, when the foot has become deformed and ulceration has occurred; TCC can be used to stabilize and support the foot, and to help move the wound toward healing.

Walking braces controlled by pneumatics are also used. Surgical correction of a joint is rarely successful in the long-term in these patients. However, off-loading alone does not translate to optimal outcomes without appropriate management of vascular disease and/or infection. Duration and aggressiveness of offloading (non-weight-bearing vs. weight-bearing, non-removable vs. removable device) should be guided by clinical assessment of healing of neuropathic arthropathy based on edema, erythema, and skin temperature changes. It can take 6–9 months for the edema and erythema of the affected joint to recede.