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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.
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.
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.
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.
Drugs like ketoconazole,
voriconazole, and itraconazole are generally employed in treating the infection. Actinomycetes usually respond well to medical treatment, but the eumycetes are generally resistant and may require surgical interventions including amputation.
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.
No vaccine is available. Simple hygienic precautions like wearing shoes or sandals while working in fields, and washing hands and feet at regular intervals may help prevent the disease.
Pentoxifylline is a useful add on treatment to compression stockings and may also help by itself. It works by reducing platelet aggregation and thrombus formation. Gastrointestinal disturbances were reported as a potential adverse effect.
Sulodexide, which reduces the formation of blood clots and reduces inflammation, may improve the healing of venous ulcers when taken in conjunction with proper local wound care. Further research is necessary to determine potential adverse effects, the effectiveness, and the dosing protocol for sulodexide treatment.
An oral dose of aspirin is being investigated as a potential treatment option for people with venous ulcers. A 2016 Cochrane systematic review concluded that further research is necessary before this treatment option can be confirmed to be safe and effective.
Oral zinc supplements have not been proven to be effective in aiding the healing of venous ulcers, however more research is necessary to confirm these results.
Treatments involve antibiotics that cover for "Pseudomonas aeruginosa". Antipseudomonal penicillins, aminoglycosides, fluoroquinolones, third generation cephalosporins or aztreonam can be given. Usually, the antibiotics are changed according to the culture and sensitivity result. In patients with very low white blood cell counts, Granulocyte-macrophage colony-stimulating factor may be given. Depending on the causal agents, antivirals or antifungals can be added.
Surgery will be needed if there is extensive necrosis not responding to medical treatments.
Athlete's foot resolves without medication (resolves by itself) in 30–40% of cases. Topical antifungal medication consistently produce much higher rates of cure.
Conventional treatment typically involves thoroughly washing the feet daily or twice daily, followed by the application of a topical medication. Because the outer skin layers are damaged and susceptible to reinfection, topical treatment generally continues until all layers of the skin are replaced, about 2–6 weeks after symptoms disappear. Keeping feet dry and practicing good hygiene (as described in the above section on prevention) is crucial for killing the fungus and preventing reinfection.
Treating the feet is not always enough. Once socks or shoes are infested with fungi, wearing them again can reinfect (or further infect) the feet. Socks can be effectively cleaned in the wash by adding bleach or by washing 60 Celsius. Washing with bleach may help with shoes, but the only way to be absolutely certain that one cannot contract the disease again from a particular pair of shoes is to dispose of those shoes.
To be effective, treatment includes all infected areas (such as toenails, hands, torso, etc.). Otherwise, the infection may continue to spread, including back to treated areas. For example, leaving fungal infection of the nail untreated may allow it to spread back to the rest of the foot, to become athlete's foot once again.
Allylamines such as terbinafine are considered more efficacious than azoles for the treatment of athlete's foot.
Severe or prolonged fungal skin infections may require treatment with oral antifungal medication.
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 first line therapy for aphthous stomatitis is topical agents rather than systemic medication, with topical corticosteroids being the mainstay treatment. Systemic treatment is usually reserved for severe disease due to the risk of adverse side effects associated with many of these agents. A systematic review found that no single systemic intervention was found to be effective. Good oral hygiene is important to prevent secondary infection of the ulcers.
Occasionally, in females where ulceration is correlated to the menstrual cycle or to birth control pills, progestogen or a change in birth control may be beneficial. Use of nicotine replacement therapy for people who have developed oral ulceration after stopping smoking has also been reported. Starting smoking again does not usually lessen the condition. Trauma can be reduced by avoiding rough or sharp foodstuffs and by brushing teeth with care. If sodium lauryl sulfate is suspected to be the cause, avoidance of products containing this chemical may be useful and prevent recurrence in some individuals. Similarly patch testing may indicate that food allergy is responsible, and the diet modified accordingly. If investigations reveal deficiency states, correction of the deficiency may result in resolution of the ulceration. For example, there is some evidence that vitamin B12 supplementation may prevent recurrence in some individuals.
Non-elastic, ambulatory, below knee (BK) compression counters the impact of reflux on venous pump failure. Compression therapy is used for venous leg ulcers and can decrease blood vessel diameter and pressure, which increases their effectiveness, preventing blood from flowing backwards. Compression is also used to decrease release of inflammatory cytokines, lower the amount of fluid leaking from capillaries and therefore prevent swelling, and prevent clotting by decreasing activation of thrombin and increasing that of plasmin. Compression is applied using elastic bandages or boots specifically designed for the purpose.
Regarding effectiveness, compression dressings improve healing. It is not clear whether non-elastic systems are better than a multilayer elastic system. Patients should wear as much compression as is comfortable. The type of dressing applied beneath the compression does not seem to matter, and hydrocolloid is not better than simple low adherent dressings. Recently there have been clinical studies on a multi-functional botanical-based ointment in combination with compression therapy in the treatment of difficult-to-heal wounds, including venous leg ulcers.
Intermittent pneumatic compression devices may be used, but it is not clear that they are superior to simple compression dressings.
It is not clear if interventions that are aimed to help people adhere to compression therapy are effective. More research is needed in this field.
Necrotic tissue should be removed in most pressure ulcers. The heel is an exception in many cases when the limb has an inadequate blood supply. Necrotic tissue is an ideal area for bacterial growth, which has the ability to greatly compromise wound healing. There are five ways to remove necrotic tissue.
1. Autolytic debridement is the use of moist dressings to promote autolysis with the body's own enzymes and white blood cells. It is a slow process, but mostly painless, and is most effective in individuals with a properly functioning immune system.
2. Biological debridement, or maggot debridement therapy, is the use of medical maggots to feed on necrotic tissue and therefore clean the wound of excess bacteria. Although this fell out of favor for many years, in January 2004, the FDA approved maggots as a live medical device.
3. Chemical debridement, or enzymatic debridement, is the use of prescribed enzymes that promote the removal of necrotic tissue.
4. Mechanical debridement, is the use of debriding dressings, whirlpool or ultrasound for slough in a stable wound
5. Surgical debridement, or sharp debridement, is the fastest method, as it allows a surgeon to quickly remove dead tissue.
The vast majority of people with aphthous stomatitis have minor symptoms and do not require any specific therapy. The pain is often tolerable with simple dietary modification during an episode of ulceration such as avoiding spicy and acidic foods and beverages. Many different topical and systemic medications have been proposed (see table), sometimes showing little or no evidence of usefulness when formally investigated. Some of the results of interventions for RAS may in truth represent a placebo effect. No therapy is curative, with treatment aiming to relieve pain, promote healing and reduce the frequency of episodes of ulceration.
The mainstay of treatment, like the treatment of gangrene, is surgical debridement, and often includes amputation.
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.
Internationally, the NPUAP, EPUAP and Pan Pacific Pressure Injury Alliance (Australia, New Zealand, Singapore and Hong Kong) published updated 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 treat pressure ulcers, including the use of bed rest, pressure redistributing support surfaces, nutritional support, repositioning, wound care (e.g. debridement, wound dressings) and biophysical agents (e.g. electrical stimulation). Reliable scientific evidence to support the use of many of these interventions, though, is lacking. More research is needed to assess how to best support the treatment of pressure ulcers, for example by repositioning.
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 lesions of digital dermatitis is done by topical application of agents to the affected skin. The skin should be cleaned and kept dry prior treatment. Topical oxytetracycline (OTC) is often referred as the most reliable treatment as cows treated with OTC have a good recovery rate. Bandaging the lesion is often undertaken but there is no evidence of any benefit and bandaging can provide the anaerobic environment which supports the spirochaetes.. Systemic antibiotics are not needed.
Control and prevention of digital dermatitis relies on prompt detection, isolation and treatment of affected cattle. Group hoof disinfection can be achieved via the passage of the cows through footbaths of antimicrobial solutions. Slurry build-up should be avoided since organic matter can impair the antimicrobial efficacy of the footbath solutions. Regular footbaths should be organised, using formalin, copper sulphate or a thymol-based disinfectant. While regular footbathing can help prevent hoof infections, occasional flare-up of active M2 lesions can happen.
Prognosis is excellent with proper treatment. Treating sexual contacts of affected individual helps break cycle of infection.
The CDC recommendation for chancroid is a single oral dose (1 gram) of azithromycin, or a single IM dose of ceftriaxone, or oral erythromycin for seven days.
Abscesses are drained.
"H. ducreyi" is resistant to sulfonamides, tetracyclines, penicillins, chloramphenicol, ciprofloxacin, ofloxacin, trimethoprim and aminoglycosides. Recently, several erythromycin resistant isolates have been reported.
Treatment failure is possible with HIV co-infection and extended therapy is sometimes required.
The main organism associated with ecthyma gangrenosum is "Pseudomonas aeruginosa". However, multi-bacterial cases are reported as well. Prevention measures include practicing proper hygiene, educating the immunocompromised patients for awareness to avoid possible conditions and seek timely medical treatment.