Evaluation and treatment of diabetic foot ulcers home,diabetic neuropathy siddha treatment of,jaren 80 verkleedkleren - Good Point

Diabetic foot ulcer is a main complication of people suffering from diabetes type 1 or type 2. Diabetes is a group of metabolic diseases characterized by high levels of sugar in the blood resulting in a deficiency in the function and secretion of the insulin.
Diabetic foot ulcer can either be from neuropathic or vascular complication of the disease. A foot ulcer usually develops on the surface of the skin or may also develop in the deeper layer of the skin. Diabetic foot ulcer generally exists in two types which are classified according to their origin while each type has their own symptoms.
Pain is often absent for most of its cases and the severity is generally rated from 0 to 3 with 0 being the mildest while 3 being the most severe in extent.
The tissues surrounding the ulcer are black in color as a result of insufficient blood flow to the affected foot. The presence of intermittent claudication is manifested by fatigue or cramping of the major group of muscles in either one or both extremities. The onset of diabetic foot ulcer is being linked to the complications of the disease in the nerve and in the blood vessels.
The treatment of diabetic foot ulcer requires bandaging or wound dressing of the affected foot.
It is also necessary to determine if the ulcer that developed is neuropathic or vascular or a combination of both in nature. Neuropathic ulcer requires protection from further injury while the wound is in the process of healing. Vascular ulcer generally requires a careful examination and evaluation from the surgeon to identify the extent of the damage whether partial or complete amputation is necessary or if amputation is necessary at all. The health information provided on this web site is for educational purposes only and is not to be used as a substitute for medical advice, diagnosis or treatment. Diabetic peripheral neuropathy is one of the most common long-term complications of diabetes.
There is no readily-available clinical gold-standard test for diagnosing peripheral neuropathy. The symptoms vary widely, depending on the specific pattern of damage to nerve fibres of different size and function. Foot deformity has a significant role in the development of pressure points in the foot which predispose it to ulceration. There may be prominence of the metatarsal heads and other bony prominences that increase the risk of skin breakdown. In a patient with diabetes, sensory loss is most often determined with the use of monofilament testing. Peripheral arterial disease is an important risk factor for the development of ulceration in the lower limbs.
To perform the test the patient is placed supine with bare feet (or their feet raised on a stool in front of the clinician). In people with acute sensory neuropathy, stabilising glycaemic levels is the primary goal of treatment. Autonomic neuropathic symptoms are likely to be present in many patients with diabetic peripheral neuropathy. Clinically there are few differentiating symptoms between the various causes of neuropathy. Neuropathy can develop as a result of the inflammatory response of the body to many immune triggers, including infection. The patient should be referred to secondary care and further testing with electrodiagnosis and CSF protein levels undertaken. Viruses and bacteria can damage nerve tissue, usually sensory fibres, leading to a painful neuropathy. In addition, neuropathy may sometimes be idiopathic (estimates are up to 20%, even in specialist centres), i.e. We treat all sort of nail problems, such as ingrown toenails, fungal toenails, thickened, blackened, bruised nails. Athlete's foot, referred to as tinea pedis by podiatrists, is a common fungal infection of the skin of your feet.
Many cases of athlete's foot can be traced to use of a public recreational facility, such as a spa, swimming pool, or locker room shower. If you can't seem to win the battle against athlete's foot, then it's probably time to visit your doctor. Athlete's foot is extremely common, and in almost all cases there is no underlying problem that led to your contracting this infection. For more information on athlete's foot treatments and to make an appointment with the NYC Athlete's Foot Podiatrist Foot Doctor, please call our office today (212) 288-3137 or click here to make an appointment. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising.
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An important first step in treating patients with diabetic foot ulcers (DFUs) is conducting a thorough evaluation of the wound bed. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Diabetic Foot Ulcers — Treatment and PreventionJarrod Shapiro1, Diane Koshimune1 and Rebecca Moellmer1[1] Western University of Health Sciences, College of Podiatric Medicine, Pomona, California, USA1. A vascular evaluation of the patient revealed multi-segmental occlusions of multiple arteries of the lower extremity, both proximal and distal to the popliteal artery. After approximately two weeks, the results of the biopsy ruled out angiosarcoma on July 5, 2006 in favor of a diagnosis of hypergranulation tissue. With the wound now revealing an overall improvement marked by decreases in depth, pain, odor and an increase in granulation, we decided to apply Apligraf on July 7, 2006. Through home health care and our nurse practitioner’s home visits, the patient’s progress was followed after the hospital discharge.
The patient’s son began questioning the ethics of the interventional cardiologist, who had also found occlusions on the contralateral lower extremity and recommended further endovascular interventions as well as periodic monitoring of the left lower extremity. Eventually, the patient developed ischemic gangrene in his right lower extremity, which resulted in a below-knee amputation. The Mayer Institute specializes in delivering world-class, evidence-based diabetic foot wound care and education. Copyright © 2012 Rachael Edwards, All trademarks are the property of the respective trademark owners. Poker228 Tempat bermain Poker paling Fair & SecureSelasa, 24 April 2012 Poker adalah Permainan Jangka Panjang dan salah satu jenis permainan kartu yang paling banyak disukai oleh Para game card, kini telah hadir poker228 yang menyediakan poker online secara real money dan fair secure. The onset of diabetic foot ulcer puts a diabetic patient at greater risk for limb loss or amputation.
The incidence of diabetes overtime can lead to various problems in health such as kidney failure, blindness and nerve damage.
A foot ulcer is characteristically a sore that develops on the surface of the skin but can also be deeper in the skin. It resembles a reddish crater that is usually located at the side or at the bottom of the foot or may be on the top or at the toe tip. The foot unlike in neuropathic ulcer is often cool to touch and the skin is thin and shiny.
No ulceration observed at the risk foot is rated as 0 while superficial ulceration with no noted infection is rated as 1. The foot is made vulnerable when it is deprived of cell oxygen due to insufficient supply of oxygenated blood. In case diabetic foot ulcer already occurred, the goal of treatment is to prevent infection and to prevent further complications including possible amputation of the affected foot. It also requires antibiotic treatment, debridement including platelet-rich fibrin therapy and arterial revascularization. The dressing can be in the form of hydrogel dressing, hydrocolloids and absorptive fillers. Identifying the nature of the ulcer will help in determining the method of treatment appropriate to the patient. Several methods of protecting and treating the wound should be strictly followed to enhance healing while frequent skin assessment is also necessary to monitor the improvement or the progression of the foot ulcer. It develops in up to half of all people with diabetes, and is one of the main risk factors contributing to foot ulceration and eventual amputation. It is important to note that a person with diabetes may have more than one form of neuropathy, e.g.
It is recommended that a monofilament is not used on more than ten patients in 24 hours, as they may buckle. Isaac Tabari, board certified (ABPM) foot & ankle surgeon treats thousands of patients every year for athlete's foot.
Isaac Tabari offers complete care for any age and cutting-edge techniques to treat foot and ankle diseases, injuries and other disorders that may be slowing your child down.
The fungus, tinea pedis, is caused by dermatophyte and is contracted from public environments. The fungus, which grows in warm, moist environments, likes to live in the outer layers of your skin. In more progressed stages of fungal infection, the toenails may become involved causing a thickened, yellowish appearance of the nail. You'll have to do this for at least several weeks, twice a day, for athlete's foot treatment to be effective.
However, fungal infections can also be an early sign of more serious problems that result in a weakened immune system. Patients with risk factors, such as neuropathy, a history of ulcers, vascular disease, or foot deformities, should be monitored more frequently.
A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population.
DFU with ischemic appearance demonstrating a yellow, fibrotic base and lack of healthy red granulation tissue.
Diabetic neuropathic plantar foot ulceration underlying tibial sesamoid bone with involved hallux valgus deformity. Acute Charcot ankle (6 weeks old) in a patient with peripheral arterial disease after sustaining a nondisplaced fibular fracture initially treated with cast immobilization. During the patient’s subsequent hospitalization, magnetic resonance imaging (MRI) and X-rays did not reveal bone marrow edema, osteolysis or deep abscess.
A biopsy of the ulcer revealed initial pathology, which triggered concern for a possible angiosarcoma. An interventional cardiologist performed subsequent revascularization using several endovascular methods including angioplasty, atherectomy, stent placement and cold laser. This improvement started to happen while further evaluation of the biopsy specimen was occurring. The patient’s son did not bring the patient to follow-up visits with the cardiologist as he verbalized the opinion that the cardiologist was only looking to “make money off” his father. The patient was admitted to a long-term care facility, where he has been residing since 2007. Bell is a board certified wound specialist of the American Academy of Wound Management and a Fellow of the American College of Certified Wound Specialists.
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Raya Centex, Ciracas, Jakarta Timur (Sederetan dengan pabrik tekstil Centex, bersebrangan dgn Alfamart Centex). The risk for amputation is increased eight fold that health professionals play a vital role in managing and preventing lower extremity ulcer among their patients. Millions of people all over the world are being affected with diabetes and it is regarded as the 7th leading cause of death.
People with diabetic foot ulcer are prone to suffer from infection due to an open wound while the ulcer generally takes longer time to heal or may not heal at all. There is also no presence of a pulse and pain while intermittent claudication and atrophy of the subcutaneous tissue can be observed. The presence of deep ulceration with an exposure of tendons or bones is rated at 2 while deep ulceration or with the presence of abscesses is rated as 3. Other symptoms of diabetic foot ulcer include ischemic pain at rest, development of non-healing ulcer or sore on the foot. In developed nations the main cause of non-traumatic lower limb amputation is “diabetic foot”, which is a result of a combination of decreased sensation and reduced arterial supply.
The fungus then grows in the warm and moist environments such as shoes, socks, locker room floors, public swimming pools, and pedicure tubs. However, for short periods of time, the fungus can live in warm puddles on the tile floor, awaiting another foot to hop onto. Untreated or severe tinea pedis could lead to painful fissuring or cracking of skin and blistering with surrounding inflammation. If you're reading this, it is likely that this particular step of treatment has either been passed, or has not worked--keep reading! If the topical antifungal treatments are not sufficient to control the problem, then an oral prescription treatment is often the next step.

This is especially true for individuals who are at risk for developing diabetes or contracting the HIV virus.
If patients have sensory loss, they should receive podiatric care and education regarding preventive foot care. A report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists.
Note the characteristic red, granular base and hyperkeratotic rim under an area of increased pressure as well as the contralateral foot with prior amputation of the 3rd, 4th, and 5th rays. Complicated diabetic wound after guillotine-type trans-metatarsal amputation treated with split thickness skin graft. Globally, diabetes mellitus has grown to pandemic proportions, affecting 194 million people worldwide and is expected to increase in prevalence to 344 million by the year 2030 [1]. The patient’s pain level decreased significantly after endovascular intervention and the ulcer responded to initial management that focused solely on regular cleaning.
He is the founder of the “Save a Leg, Save a Life” Foundation, a multidisciplinary, non-profit organization dedicated to the reduction of lower extremity amputations and improving wound healing outcomes through evidence-based methodology and community outreach. Diabetic foot ulcer is among the problems or complications that can arise from chronic disease which makes an affected individual at high risk of losing a limb.
When an infection occurs, a pocket of pus and cellulitis may develop including bone infection. People with peripheral neuropathy is unable to perceive pain when they stepped on something sharp or when their feet is in discomfort or when the feet is already injured or wounded unless given a closer look.
Assessing for peripheral neuropathy is a routine part of ongoing care for patients with diabetes. Athlete's foot can be transmitted to the skin through a cut or abrasion on the bottom of the foot. Once you do get rid of athlete's foot, you're going to want to know how to prevent it from happening again in the future. There are quite a few antifungal medications on the market, your doctor will help you decide which is best.
If someone in your family has diabetes, or if you are at-risk for HIV (high-risk sexual activity, needle sharing), then you should see your doctor to confirm that these are not potential underlying disorders. Data Points #3 (prepared by the University of Pennsylvania DEcIDE Center, under Contract No.
Clinical presentation and initial evaluationAs in all medical conditions the initial evaluation of a patient with a diabetic foot ulcer begins with a detailed history. While awaiting the second assessment of the biopsy assessment, intensive wound care included daily pulsed lavage, IV antibiotics and an alginate dressing saturated with Dakin’s solution. Gangrene may later occur which can lead to poor circulation subsequently amputation or a loss of a limb.
Fortunately, some of the newer medications have minimal side-effects and are less expensive, but because of possible complications all of the oral antifungals are available only by prescription. The onset of a DFU often precipitates a complex chain of events that may lead to limb loss. In the case of nerve that is not functioning, the pain is not felt and the presence of the foot ulcer may not be noticed. The long-term outcome for a diabetic patient after a major limb amputation is grave, with 50% of these patients deceased at 5 years [3]. On physical examination one may appreciate the classic appearance of the diabetic plantar foot ulcer (Figure 1).
The difficulty with diabetic patients is their lack of systemic response due to immunopathy, where leukocytosis may be absent. In the United States public discussion and much research money goes to the investigation and treatment of breast and prostate cancers. This is most commonly a partial or full thickness wound underlying a bony prominence or area of deformity. However, in a subset of patients elevation of white blood cells (WBC) may be found at initial presentation.
However, when the 5 year mortality percentages are analyzed, a diabetic neuropathic ulcer has a worse survival rate than each of these cancers. When chronic low grade elevated plantar pressures are present the skin forms reactive hypertrophic tissue, indicated by hyperkeratotic callus, the tell-tale sign of the neuropathic ulcer.
Recent studies have shown that C-reactive protein (CRP) is the most sensitive and specific lab test to distinguish between grade 2 and grade 1 ulcers [71].Plain radiographs can provide useful information in the presence of a diabetic foot ulcer when there is suspected soft tissue emphysema. Dengan system teknology baru dan server kecepatan tinggi akan membuat permainan poker anda lebih seru dan menarik bersama teman2x anda maupun saingan anda.
The wound should be examined for size, undermining (in which the edges of the wound overlap the base), general appearance, and the probe to bone test should be performed. Advanced imaging techniques such as magnetic resonance imaging (MRI) can provide information regarding the extent of tissue and bone involvement [58, 61, 63, 69]. In fact having a neuropathic ulcer or prior amputation has the same poor survival rate as colon cancer [4]. Note the characteristic red, granular base and hyperkeratotic rim under an area of increased pressure as well as the contralateral foot with prior amputation of the 3rd, 4th, and 5th rays.During this test the examiner uses a sterile metal probe (often the blunt end of a cotton swab is used) to gently but firmly push into the base of the wound. TreatmentThe consensus from multiple studies and practice guidelines is to utilize a multi-disciplinary approach, including providers from primary care, endocrinology (diabetologist), podiatry, vascular surgery, plastic surgery, infectious disease, microbiology, wound specialty nursing, physical therapy, orthotist and prosthetists [43, 58, 59, 61, 63, 69, 72, 73]. It is unknown if the lower extremity complications themselves lead to greater mortality, but it may be assumed that complications such as a foot ulcer are indicators of more significant diabetic disease with its well-known increased risk of cardiovascular complications.This chapter will focus on key concepts related to prevention and treatment of diabetic foot ulcers and their complications. The examiner then determines the depth to which the probe may go, whether to subcutaneous, capsular, or bone layers.
However, there is no evidence-based consensus on specific treatment algorithms for soft tissue infections. If the probe is able to touch bone this is considered a positive probe to bone test and is highly predictive of osteomyelitis. Unfortunately any attempt at making such a consensus based on existing data is challenged by inconsistent definitions of infection, improvement and cure, and patient to patient variability.
A rational approach to the evaluation and treatment of diabetic foot ulcers will be discussed, utilizing the most current research.2. Therapy is typically guided by knowledge of likely pathogens, based on history and clinical presentation and spectrum of available antibiotics that can reliably provide coverage [58]. Pathogenesis of the diabetic foot ulcerThe diabetic foot ulcer is a complex multifactorial entity with a well-known etiologic pathway. In patients with severe infection and a higher likelihood of osteomyelitis, this test has a positive predictive value of 89% [15].
Patients who have a Grade 2 non-limb threatening infection should be treated on an outpatient basis, covering for gram-positive cocci, and reassessed in 48-72 hours. If the infection has not improved the patient should be admitted for parenteral antibiotics and possible incision and drainage.
Brand discussed the concept of “tenderizing” the foot [7] in which peripheral neuropathy leads to a loss of function of two types of mechanoreceptors in the skin, responsible for delivering nociceptive signals. Patients with grade 3-4 infections that are considered limb- or life- threatening should be admitted for parenteral antibiotics and incision and drainage. High threshold mechano-receptors, carried via A-delta fibers, normally become sensitized to increased repetitive pressures on healthy tissues. In this situation the inability to palpate bone with the probe indicates a low likelihood of osteomyelitis.A thorough physical examination should also include an evaluation of arterial outflow and the presence of peripheral arterial disease (PAD). Caution should be exercised as approximately half of the patients in this category will not mount an immune response. This sensitization lowers the pain threshold in the patient with normal sensation, carried by polymodal nociceptors, leading to altered behaviors which reduce pain and subsequent damage. Therapy should be broad spectrum, including coverage for gram negative rods and anaerobes [59] in addition to gram positive cocci. In the neuropathic patient this sensitization system is absent, allowing tissue damage to occur without any pain response with the subsequent diabetic foot ulcer.Diabetic peripheral neuropathy also causes motor and autonomic dysfunction. The absence or diminution of a peripheral pulse (specifically the dorsalis pedis or posterior tibial) has a sensitivity between 63% and 95% and a specificity between 73% and 99% for peripheral arterial disease [17-19]. A familiarity with antibiotics available in specific hospital formularies and profiles of microbial resistance patterns (via antibiogram) will improve targeted therapies. It was previously thought that parenteral antibiotics were necessary initially for all severe infections.
As the intrinsic pedal musculature becomes poorly functional muscular imbalances occur causing deformity. However studying the high serum concentrations achieved with oral forms of some antibiotics such as Linezolid and trimethoprim-sulfamethoxazole, for example, suggest that intravenous administrations may not always be necessary [58].
This deformity allows for focal areas of increased pressure, becoming risk areas for ulceration.
Autonomic neuropathy contributes via sudomotor dysfunction causing loss of sweat glands as well as loss of nutritive supply with subsequent dry skin that breaks down easily [5]. Trophic changes of the skin may include atrophic, shiny appearance with loss of hair, coolness to touch, cyanosis, and thickened nails.
Mild infections warrant a short course of 1-2 weeks, while moderate to severe infections can require up to 2-4 weeks of targeted therapy. An ill-fitting pair of shoes may be all that was required for the shear forces to lead to an ulceration of a patient’s foot who has diminished sensation.If skin breakdown and wound formation occurs by a combination of high pressures in the insensate foot then wound chronicity is upheld by altered and inappropriately functioning biochemical pathways and chemical mediators. Trophic changes generally have a lower sensitivity and specificity for PAD [17].In the diabetic patient with a neuropathic foot ulcer and concomitant PAD the wound appearance may be slightly different. Inflammatory markers such as CRP and erythrocyte sedimentation rate (ESR) are used to define duration of therapy [58].
Various cytokines and matrix proteins have been implicated in the process of delayed wound healing.
In some situations the wound will look similar to the well vascularized ulcer with the exception of a more pale or light pink appearance to the wound base instead of a red, granular appearance. One of these mediators that has received much emphasis over the recent past is matrix metalloproteinase 8 (MMP-8), which is the primary collagenase in normal wounds [9]. In more advanced neuroischemic wounds the appearance will be markedly different with a fibrous yellow appearance and an often irregular, sometimes punched out-appearing, shape (Figure 2). In chronic wounds MMP-8 is upregulated due to reduction of its regulating enzyme TIMP-1 (tissue inhibitor of metalloproteinase 1).
Although ertapenem did not provide specific coverage for Pseudomonas or Enterococcus species, at the end of the therapy period the success rate for both groups of patients was similar.
This overexpression of MMP-8 causes enzymatic destruction of the wound extracellular matrix, thus retarding wound healing. In the majority of patients an examination of the biomechanical contribution will reveal the cause of the ulcer. This raises the question of whether certain bacteria such as Pseudomonas and Enterococcus require antibiotic coverage. The diabetic foot ulcer may also be lacking growth factors such as platelet-derived growth factor (PDGF) and tumor growth factor beta (TGF-?) which stimulate fibroblast proliferation and synthesis and act as chemoattractants for neutrophils, smooth muscle cells, and macrophages [10] in the healthy wound. These organisms are colonizers and become primary pathogens in very specific instances, acting as opportunistic pathogens.
In order to prevent further propagation of multi-drug resistant organisms, practitioners should choose antibiotics with slightly narrower coverage [58, 60, 74].Occasionally soft tissue infections accompanied by abscess, substantial necrosis or necrotizing fasciitis require surgical debridement in addition to broad spectrum, followed by targeted, antibiotic therapy.
Overall appearance of the foot should be appreciated, followed by a detailed examination of specific deformities, including joint position, range of motion, and rigidity versus flexibility (Figure 3). Risk factorsSeveral clinical causal pathways have been researched, allowing the clinician to grade the primary risk factors associated with the onset of DFUs. For moderate to severe diabetic foot infections, surgical intervention is often the key to limb salvage [69].
Lavery et al, described an update to the clinical staging method previously proposed by the International Working Group for the Diabetic Foot [11, 12]. For example, lack of motion of the great toe joint (hallux limitus) often leads to a compensatory increased motion at the hallux interphalangeal joint. The incision should be centered on the abscess and extended proximally until there is no evidence of infection.
Table 1 demonstrates increasing trend of ulceration, infection, and amputation, with an extremely high risk of hospitalization with increasing stage. This compensation increases plantar pressures at the joint with a subsequent DFU (Figure 4).
Non-viable tissues can be debrided, and exposed tendons and bone can be removed in preparation for eventual closure [72]. There are three methods for wound closure: primary, delayed primary and closure by secondary intention.
Plantar pressures have been shown to be increased three fold in diabetic patients with ankle equinus when compared with those without [21]. Primary closure can be achieved when the surgeon is confident the necrotic tissue and infection has been removed using a combination of sharp debridement and lavage.
The monofilament is constructed to produce a standard 10 grams of force when bent and has been found to accurately predict the presence of ulceration [13]. The relationship between callus and ulceration was confirmed by Murray and colleagues who found a relative risk of 11.0 for an ulcer developing under an area of callus [22].
However, in cases of severe infection or when there is suspicion for additional drainage to be encountered, a wound may be left open initially then closed several days later when it is free of any signs of infection –delayed primary closure. As such, the relationship between ankle equinus, increased plantar pressures, and DFU is well established.

Finally, for those wounds with significant undermining or other potential complicating factors, closure by secondary intention may be undertaken in which a wound is left open and allowed to granulate or contract, often with the help of advanced modalities such as NPWT, split thickness skin grafting or other synthetic graft materials [59, 72]. If the patient is unable to feel 4 of 10 sites, he is diagnosed with peripheral neuropathy.
Upon completion of the physical examination, laboratory and imaging methods may be employed in certain circumstances to better appreciate the underlying anatomy and will be discussed below.A simple, rapid examination of the foot takes no more than one to two minutes. From a clinical standpoint a significant sign of impending ulceration is the preulcerative callus.
When superficial infections are encountered physicians should aggressively treat them to prevent progression and involvement of deeper or wider margins of tissue. This is seen as hyperkeratotic tissue with visible hemorrhage within the epidermal or dermal skin layers.
Some infections warrant early surgical debridement, which can reduce morbidity and cost [63]. Treatment of diabetic foot ulcerations can be intimidating and complex without a basic understanding of the treatment options available and a thorough evaluation of the ulcer’s characteristics. When amputations are considered, they should be performed as far distal as possible as there are higher energy expenditures and disturbance to quality of life with proximal amputations. Current literature suggests that, if the initial treatment plan does not reduce the size of the ulcer by 50% in four weeks that the course of treatment should be re-assessed [23-26].
In paraplegic and quadriplegic patients or other patients who are otherwise non-ambulatory, surgical planning should take into account the future risk of complications such as decubitus or neuropathic ulcerations, contractures or infection [59]. Essential components of any initial or re-evaluated treatment plan should consist of debridement, moist wound healing environment, offloading and infection control [27]. Conservative options are typically employed initially [28] but if progress stalls, surgical components to the treatment plan may help to decrease time to healing or even promote healing. Characteristics of the diabetic foot ulcer are important to consider because they directly influence what treatment modalities are used. OsteomyelitisOccasionally, soft tissue infections can be severe and deep, involving underlying bony structures. Evaluation of the diabetic foot ulcer’s location, size and depth, tissue type, presence or absence of drainage, length of time the ulcer has been present, vascular supply, and any pathomechanics present are all important variables when formulating the treatment plan. When there is a break in the soft tissue, and the infective organisms have entered the bone directly, this is referred to as contiguous or direct extension osteomyelitis [15, 61, 75]. DebridementThe type of tissue found within the diabetic foot ulceration is an important treatment consideration. Other types of osteomyelitis include hematogenous osteomyelitis which is seen in prepubescent children and in elderly patients in which spread occurs through the blood [75]. When yellow fibrotic tissue or dusky necrosis is noted, steps must be taken to covert the diabetic ulcer base to a beefy, red, healthy granular tissue.
Surgical debridement of avascular tissue may improve rates of ulcer closure by removing the tissue that had served as a foreign body.
PathogenesisInfections in the bone are initiated by adhesion of bacteria in the acute osteitis phase followed by firm attachment, which is the chronic phase. Several types of debridement are commonly employed today but there is no scientific evidence suggesting that one type is superior to another [29, 30] only that diabetic foot ulcers receiving a regular debridement are found to heal faster [30]. The adhesions are formed through a polysaccharide capsule that links strongly to the bone matrix. Debridement is a necessary step that prepares the wound bed to promote healing [30] and is helpful when converting a chronic wound to an acute ulcer [25]. Sharp debridement is considered the gold standard [30, 31] and can be performed at the bedside or in the operating room [32]. Enzymatic debridement, such as collagenase for fibrotic tissue is a good option when the risk of debriding small quantities of healthy tissue is not acceptable or if the patient experiences pain with sharp debridement. Hydrosurgical debridement, as with Versajet® (Smith and Nephew corporation), demonstrates no statistically significant reduction in bacterial contamination [33] and was found only to decrease the duration of time spent debriding the ulcer [31]. In reaction to the bacterial antigens, the body will also produce interleukin-1 (IL-1) and tumor necrosis factor-? (TNF-?) which result in an increase in osteoclast-mediated osteolysis [60, 62].As mentioned above, emergence of drug resistant organisms is a large problem facing healthcare providers today.
Biologic debridement, using medically sterilized Lucilia sericata larvae, aims to rid the ulcer of necrotic tissue and pathogens [30, 34]. It has been shown that gradual exposure of antibiotics through the biofilm layers can result in resistance as the organisms are able to tolerate 10-1000 times higher levels of antimicrobial agents in comparison to the minimum inhibitory concentration. However, maggot therapy has not demonstrated improvement of healing rate or reduction of bacterial load as compared with hydrogel [29, 30]. Applying hydrogel or hydrocolloid dressings introduces moisture, and if placed under occlusion, serves as a form of autolytic debridement that allows the body’s own enzymes to liquefy necrotic tissue.
Hydrogel, additionally, has been found to increase the rate of healing as compared with plain gauze [29]. Mechanical debridement, also known as “non-selective debridement” is performed by applying saline moistened gauze to the ulcer and allowing it to dry before the dressing is periodically changed. The removal of the gauze mechanically removes both healthy and unhealthy tissue and is no longer considered the best dressing for diabetic foot ulcers [26].The size and depth of the diabetic foot ulcer are important factors to evaluate because a deep ulcer may have avascular tissue such as tendon exposed. Instead of allowing the avascular tissues to desiccate and require debridement, potentially losing long-term function in the foot, immediate use of a negative pressure wound therapy (NPWT) system has been shown to increase volume of granulation tissue within the ulcer [29, 35, 36] which may possibly preserve that structure. NPWT has also been shown to significantly improve the rate of wound closure as compared to simple saline gauze dressings [26, 29, 37] and NPWT has demonstrated a reduced amputation incidence [26] and decreased hospital stay [38]. Ultrasound, lasers, electrical and electromagnetic therapies have been evaluated in laboratory research but there is insufficient evidence to suggest these have any effect on diabetic foot ulceration healing times [29]. Clinical evaluationThorough history of patients who present with suspected osteomyelitis should be performed in addition to a thorough physical exam as previously discussed. Moist wound healing environmentThe presence or absence of drainage helps to determine what type of adjunct dressing the diabetic foot ulcer may require. Lab evaluationComplete blood count is of limited usefulness in diagnosing osteomyelitis as leukocytosis is infrequent [62, 75]. By converting a chronic diabetic foot ulcer to an acute wound and maintaining a moist wound bed, the inflammation, infection and exudate are controlled while increasing epithelial advancement [25, 34]. This prevents retardation of cellular proliferation and angiogenesis by eliminating the excessive levels of matrix metalloproteinase’s, growth factors and cytokines [34] present in the chronic wound. Unlike in metastatic or metabolic bone diseases, the serum calcium, phosphate and alkaline phosphatase all remain normal [75]. If excessive drainage is present an absorbent dressing should be used, such as a calcium alginate or another absorbent fiber.
Other dressing components have been found to increase healing in small studies such as the use of topical and oral ?-glucan [39].
In another study, comparison of various dressing options demonstrated no statistical difference in ulcer healing but did note that the basic wound contact dressing, was more cost-effective in healing diabetic foot ulcers than a fibrous hydrocolloid dressing [40].If the diabetic foot ulcer has been present for 30-90 days [35] it is considered chronic. Chronicity may dictate whether or not to use bioengineered products that deliver fibroblasts superficially, such as Dermagraft® (Advanced Tissue Sciences), Apligraf (Organogenesis) or healthy doses of growth factors, such as platelet rich protein gel delivered superficially.
Both, Dermagraft® and Apligraf®, used with effective offloading, have demonstrated decreased healing time [41, 42] and several studies suggest that utilization of near-physiological concentration of platelet rich protein gel on recalcitrant or chronic wounds demonstrate a rapid and consistent healing [32, 34, 35, 43] and is cost-effective [42]. A smaller study suggests that injected, rather than topical, epidermal growth factor at the lesion’s base may result in improved healing [44] due to elimination of high levels of proteases that reduce levels of growth factors needed for healing [34]. OffloadingThe location of the diabetic foot ulcer is commonly found overlying a bony prominence [25, 34] or involving a deformity (Figure 5). Total contact casting (TCC) (Figure6A ), is considered the best method of offloading as compared to a removable walking cast [27].
When these conservative means for offloading are ineffective, surgical resection of the underlying bony prominence, termed internal off-weighting, is an option [25].
This surgical treatment may entail bony procedures such as an exostectomy, condylectomy, arthroplasty [25, 36], metatarsal osteotomy [28] or arthrodesis [28]. Additionally, tendon transfers to rebalance the foot and amputation may also be applied as indicated (Figure 7).Surgical procedures should be chosen and performed by those with expertise in surgical reconstruction of the diabetic foot and ankle. Pathomechanics of the patient’s foot, such as gastrocnemius-soleus equinus or a taut plantar fascial ligament both leading to plantar forefoot ulcerations, may necessitate conservative offloading measures as previously mentioned. However, if the offloading attempts are ineffective, a surgical release (plantar fascial ligament resection [28, 46, 47]) or surgical lengthening (tendo-achilles lengthening [25, 28, 46, 48]) of the contracture may allow the forefoot to be more flexible when met with ground reactive forces thus healing the diabetic plantar foot ulcer [49].
Mueller et al’s randomized clinical trial found that patients treated with a tendo-achilles lengthening and a TCC were 12% more likely to heal a plantar foot ulcer than with a TCC alone. Additional methodsVarious types of skin grafts and flaps may assist with closure of the ulceration (Figure 8) as healing an ulcer by means of secondary intention represents a major burden to patients, health care professionals and the health care system [50]. Bioengineered skin grafts and split-thickness skin grafts do not show statistically significant success in healing diabetic foot ulcers [29] despite small studies suggesting grafts improve rates of healing and decreased evidence of amputations [51, 52].
Local muscle flaps have also been found to be successful in closing complicated diabetic foot wounds and are far superior as compared to the survival rates of amputees [53].
Despite an increased complication rate, pedicled flaps were found to have comparable limb salvage success as compared with free flaps [53]. Successful healing.Hyperbaric oxygen (HBO) therapy systemically has been found to decrease the rate of major amputations [29] but not in the rate of minor amputations [54]. When a conservative treatment plan is found to improve the ulcer but does not heal it, utilizing HBO therapy may help to increase the partial pressure of oxygenation to tissues and help heal the wound [54, 55]. A study has demonstrated that the use of HBO facilitates wound closure when there is a change in transcutaneous oxygen measurements of ? 10 torr [56]. Topical hyperbaric oxygen therapy has not been found to decrease the rate of major amputations [29] and cannot be recommended for use in diabetic foot ulcers at this time. When various treatment modalities are not successful, if possible, a limb salvage attempt is advised. External fixation is an additional option, boasting skeletal stability, easy access for soft tissue management, and assisting with plastic surgery wound closure techniques [36, 57].
If external fixation is not available or possible, there are many levels of amputations to consider [36]. While a trans-tibial amputation has the same long-term survivorship as some mid and rearfoot amputations (Symes, Lisfranc, calcanectomy or Chopart’s) a partial foot amputation allows higher ambulatory levels and longer durability with less morbidity and mortality than trans-tibial amputations [51].
Allowing the patient to have a good quality of life, maintain as much function as possible and increase ease of prosthetic use following the amputation are important advantages to consider.5.
InfectionOne of the earliest complications of diabetic foot ulcerations is infection [58] and if not treated adequately, may require amputation. This of particular concern because the 3 year survival rate following a lower limb amputation is 50%, decreasing to only 40% after 5 years [59].All skin surfaces, and thus all wounds, have a certain level of bacteria on the surface at baseline, referred to as surface contaminants, defined as bacteria which are present but do not multiply. Whether the bacteria are able to surmount a response from the host immune system will dictate whether there is an infection. Some believe that observing 105 bacteria per 1 gram of tissue is the threshold between a colonizer and an established infection. However, depending on the bacterial species or strain, an infection can result with far fewer than the 105 bacteria per 1 gram of tissue. Take for example ?-hemolytic streptococci, which produce enzymes that promote tissue invasion and cause progressive infections without the same bacterial burden as other organisms [58, 60-62].Risk factors for infection include a non-healing ulcer, advanced age, male sex, black race and a history of smoking in addition to sensory and autonomic neuropathy [63]. Diabetic foot infections are difficult to manage due to the associated comorbidities affecting the patient such as neuropathy, peripheral vascular disease, immunopathy and nephropathy [59]. Organisms such as methicillin resistant strains of Staphylococcus aureus, among others, pose a challenge to healthcare providers. Several factors such as prolonged hospital stays, exposure to surfaces and personnel who may have come into contact with resistant strains, and prolonged or prior antibiotic treatment can result in infections with these organisms.
Many patients with chronic ulcerations have a history of recurrent ulcerations and infections that place them at high risk for infection with resistant organisms [65]. Poor glycemic control has been connected to impairment in leukocyte phagocytosis and chemotaxis, which increase the risk for infection. Clinical findingsPatients with infections typically present with erythema, edema, purulent drainage, malodor, calor, induration, lymphangitis, soft tissue edema and occasionally gangrene or necrotic tissue (Figure 9). Patients also complain of recalcitrant hyperglycemia and other constitutional symptoms such as fevers, malaise and chills, sometimes referred to as the ‘diabetic flu’, which should raise suspicion for a deep infection [59, 61, 68]..
Superficial infections typically show no signs of systemic toxicity and glycemic levels remain unaffected.
Deep foot infections, in contrast, result in contiguous spread of erythema and edema with accompanying constitutional symptoms such as fever, chills, malaise, and occasionally blood glucose elevations.
DiagnosisIdentification of infecting organisms for diabetic foot wounds is of great interest, particularly when considering antibiotic therapies. Depending on the chronicity of the wound there can be a slight difference in the organisms that can be isolated from a wound culture. Acute wounds typically grow gram positive cocci while chronic wounds are polymicrobial, with a mixture of gram positive cocci, gram negative bacilli and anaerobic organisms (Table 2) [58, 69, 70].
Those patients who have been previously hospitalized or have had prolonged antibiotic therapy can have an altered profile of organisms.
Patients who have not been on any recent antibiotics typically grow gram positive organisms with a greater likelihood of gram negative organisms and organisms that are resistant to antibiotics [65]. Instead, deep tissue specimens should be taken from the wound after a sharp debridement either with a scalpel or curette. Alternatively, in the presence of an abscess, aspiration of the abscess can provide more accurate information regarding the infecting organisms [58, 61, 63, 64].

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