Diabetic foot ulcers are the major complications of diabetes mellitus, and may be a major component of the diabetic foot.
Wound healing is a mechanism of innate action that works reliably most of the time. A key feature of wound healing is the gradual improvement of the missing extracellular matrix (ECM) that makes up the largest component of the skin layer. But in some cases, certain disorders or psychological disturbances interfere with the wound healing process. Diabetes mellitus is one of the metabolic disorders that inhibits the normal step of wound healing process. Many studies show a prolonged inflammatory phase in diabetic wounds, which causes delays in the formation of mature granulation tissue and parallel reduction in tensile strength.
Treatment of diabetic foot ulcers should include: blood sugar control, removal of dead tissue from wounds, wound dressings, and removal of pressure from the wound through techniques such as total contact casting. Surgery in some cases can improve outcomes. Hyperbaric oxygen therapy may also be helpful but expensive.
This occurs in 15% of diabetics, and precedes 84% ​​of all diabetes underfoot amputations.
Video Diabetic foot ulcer
Classification
Diabetic foot ulcers are a complication of diabetes. Diabetic foot ulcers are classified as neuropathic, neuroischaemic or ischemic.
Maps Diabetic foot ulcer
Risk factors
The risk factors involved in the development of diabetic foot ulcers are infection, older age, diabetic neuropathy, peripheral vascular disease, smoking, poor glycemic control, previous leg ulceration or amputation, and small and large vessel ischemia. Previous history of foot disease, foot deformities resulting in abnormally high pressure pressures, renal failure, edema, impaired ability to maintain personal care (eg visual impairment) are further risk factors for diabetic foot ulcers.
People with diabetes often develop diabetic neuropathy due to several metabolic and neurovascular factors. Peripheral neuropathy causes loss of pain or feeling in the toes, legs, legs and arms because of distal neural damage and low blood flow. Blisters and cuts appear in the numbness areas of the feet and feet such as the metatarso-falangeal joints, the heel area and as a result undetectable pressure or injury and eventually become the entrance for bacteria and infections.
Pathophysiology
Extracellular matrix
An extra cellular matrix (or "ECM") is an external structural frame attached to cells in multicellular organisms. The dermis lies beneath the epidermis, and these two layers are collectively known as skin. Dermal skin is primarily a combination of fibroblasts that grow in this matrix. ECM specific species of connective tissue often differ chemically, but collagen generally forms most of the structure.
Through cell interactions with an extracellular matrix (transmitted through anchoring molecules classified as integrins) there forms a continuous relationship between interior cells, cell membranes and extracellular matrix components that help to drive various cellular events in a regulated way. Wound healing is a local event involving cell reactions to sustained damage.
The cells break down the damaged ECM and replace it, generally increasing in number to react to hazards. This process is enabled, though not exclusively, by cells that respond to damaged ECM fragments, and improvements are made by rearranging the matrix by the cells that grow and through them. Because this extracellular matrix is ​​often regarded as a 'wound healing symphony conductor'. In the inflammatory phase, neutrophils and macrophages recruit and activate fibroblasts which in the next granulation phase migrate into the wound, putting new collagen from subtype I and III.
In the early incidence of wound healing, collagen III dominates the granulation tissue which then in the remodeling phase is replaced by collagen I provides additional tensile strength to the healing tissue. It is evident from the collagen assembly known that tensile strength is essentially due to the fibrillar arrangement of collagen molecules, which self-assemble into longitudinal and lateral microfibrils that produce extra strength and stability in collagen assembly. The metabolically modified collagen is known to be highly inflexible and susceptible to damage, especially in pressure areas. Fibronectin is the main glycoprotein secreted by fibroblasts during the initial synthesis of extracellular matrix proteins. This serves importantly, being chemo-attractant for macrophages, fibroblasts and endothelial cells.
The basal membranes that separate the epidermis from the dermal layer and the endothelial basement membrane primarily contain collagen IV forming the sheets and bind to other extra cell matrix molecules such as laminin and proteoglycans. In addition to collagen IV, epidermal and endothelial basement membranes also contain laminin, perlecan and nidogen. Hyaluronic acid, a pure glycosaminoglycan component found in high amounts in damaged or growing tissue. It stimulates cytokine production by macrophages and thus promotes angiogenesis. In the normal skin of chondroitin sulfate proteoglycan is mainly found in basement membranes but in wound healing they are arranged throughout the granulation tissue especially during the second week of wound repair, when they provide a temporary matrix with a very hydrating capacity. Binding of growth factors is clearly an important role of perlecan in wound healing and angiogenesis. Poor wound healing in diabetes mellitus may be associated with perlecan expression. High levels of glucose can decrease perlecan expression in some cells possible through transcriptional and post-transcriptional modification. The phase of wound healing mainly, granulation, re-epithelialization and remodeling shows the controlled cycle of the extracellular matrix component.
Changes in metabolism
Diabetes mellitus is a metabolic disorder and hence the defect observed in diabetic wound healing is considered as a result of changes in protein and lipid metabolism and thus the formation of abnormal granulation tissue. Increased levels of glucose in the body end up with uncontrolled algal covalent sugar bonds into proteins or lipids without normal glycosylated enzymes. This stable product then accumulates over the surface of cell membranes, structural proteins and circulating proteins. These products are called advanced glycation endproducts (AGEs) or Amadori products. The formation of AGEs occurs in extracellular matrix proteins with slow turnover rates. AGEs alter the properties of matrix proteins such as collagen, vitronectin, and laminin through the AGE-AGE intermolecular covalent bonds or cross-linkages. AGE cross-linking in type I collagen and elastin results in increased stiffness. AGEs are also known to enhance the synthesis of collagen type III which forms the granulation tissue. AGEs in laminin yields reduced binding to type IV collagen in the basement membrane, reducing polymer elongation and reducing proteoglycan binding of heparan sulphate.
- NO synthesis disorder
Nitric oxide is known as an important stimulator of cell proliferation, maturation and differentiation. Thus, nitric oxide increases the proliferation of fibroblasts and thus the production of collagen in wound healing. Also, L-arginine and nitric oxide are required to connect precise crosslinking of collagen fibers, through proline, to minimize scarring and maximize the tensile strength of the healed tissue. The synthesis of nitric oxide-specific endothelial cell oxide (EcNOS) is activated by blood flow through pulsating blood vessels. Nitric oxide produced by EcNOS, maintains the diameter of blood vessels and proper blood flow to the tissues. In addition, nitric oxide also regulates angiogenesis, which plays a major role in wound healing. Thus, diabetic patients exhibit a reduced ability to produce nitric oxide from L-arginine. Reasons that have been postulated in the literature include the accumulation of nitric oxide inhibitor synthase due to high glucose linked renal dysfunction and decreased production of nitric oxide synthase due to ketoacidosis observed in diabetic patients and the dependent properties of nitric oxide pH synthase.
- Structural and functional changes to fibroblast
Diabetic fibroblast ulcers show a variety of morphological differences compared to fibroblasts of age-matched controls. Diabetic fibroblast ulcers are usually large and widespread in the culture flasks compared with spindle morphologies of fibroblasts on age-appropriate controls. They often show dilated endoplasmic reticulum, many vesicular bodies and lack of microtubule structures in transmission electron microscopy studies. Therefore, the interpretation of this observation is that regardless of the production of high protein and protein turnover in diabetic ulcers fibroblasts, vesicles containing secretory proteins can not travel along microtubules to release products outside. Fibroblasts from diabetic ulcers show proliferative damage that may contribute to decreased production of extracellular matrix proteins and delayed wound contractions and wound healing disorders.
- Increased matrix activity of metalloproteinase (MMP)
In order for wounds to heal, extracellular matrix not only needs to be established but also must be degraded and remodeling to form adult tissue with appropriate tensile strength. Protease, the metalloproteinase matrix, is known to degrade almost all components of the extracellular matrix. They are known to be involved in the migration of fibroblasts and keratinocytes, tissue rearrangement, inflammation and remodeling of injured tissue. Because of the high concentrations of pro-inflammatory cytokines in diabetic ulcers, MMP activity is known to increase 30-fold when compared with acute wound healing. MMP-2 and MMP-9 show continuous overexpression in chronic diabetic ulcers that can not cure. The balance in MMP activity is usually achieved by tissue inhibitor metalloproteinase (TIMP). Rather than the absolute concentration of both, it is the ratio of MMP and TIMP that maintain a proteolytic balance and this ratio is found to be impaired in diabetic ulcers. Regardless of these findings, the exact mechanism responsible for increased MMP activity in diabetes is unknown. A line of thought that might consider Transforming growth factor beta (TGF-?) As an active player. Most MMP genes have TGF-? an inhibitory element in their promoter region and thus TGF-? regulate the expression of MMP and TIMP inhibitors. In addition to the importance of cell interactions and cell matrices, all wound healing phases are controlled by different growth factors and cytokines. To pinpoint, growth factors promote the transition of the initial inflammatory phase to the formation of granulation tissue. The fall of growth factor responsible for tissue repair like TGF-? documented in a diabetic injury. So, reduce the TGF level? in the case of diabetes decreases the effect of inhibitory regulatory effects on the MMP gene and thus causes MMP to overexpress.
Biomechanics
Complications of the diabetic foot and ankle-ankle complex are wider and more damaging than expected, and may compromise the structure and function of some systems: vascular, nervous, somatosensory, musculoskeletal. Thus, a deeper understanding of gait and foot biomechanics changes in the legs of diabetes is very interesting, and may play a role in the design and initiation of preventive and therapeutic measures.
In summary, the effect of diabetes on the main structure of the foot-ankle complex can be summarized as: The effects of
- on the skin: the skin - and soft tissue immediately under the skin - experience greater compression and shear loading than usual, thus explaining the occurrence of tissue damage that is highly correlated with the process of traumatic ulcers. In addition, diabetic foot skin suffers from loss of autonomic nerve control and consequently reduces hydration, resulting in less elasticity and is therefore more susceptible to increased mechanical stress action;
- effects on tendons and ligaments: protein glycosylation and resulting collagen abnormalities lead to larger transverse portions - ie larger tendons and ligaments and coefficient of elasticity. The most affected by this process are Plantar Fascia and Achilles Tendon. Both causes cause an increase in the stiffness of the structure;
- The effect on cartilage: similar to what happens to the tendons and ligaments, the cartilage alters its composition mainly due to the modification of collagen fibers. This increases his stiffness and decreases the range of motion of all joints in the legs and ankles.
- Effect on muscle: Diabetes mellitus causes severe damage to nerve conduction, thus causing deterioration in the management of related muscle fibers. As a result, both intrinsic and extrinsic muscles of the foot-ankle complex are damaged in structure (muscle volume reduction) and function (muscle strength reduction); Effects of
- on peripheral sensory systems: nerve conduction disorder has a dramatic effect on the peripheral sensor system, as it causes a loss of protective sensation under the sole of the foot. It exposes the diabetic foot for thermal or mechanical trauma, and for late detection of infection processes or tissue damage;
- the effect on foot morphology (disability): due to most of the above changes, a significant imbalance of peripheral and soft tissue muscles occurs in the foot that seriously alters its morphology and determines the onset of foot deformity. The most common deformity of the diabetic foot is represented by a high longitudinal arch (rigid cavus leg), hammer and hallux valgus. An entirely different morphological degeneration is represented by neuropathic arthropathy, whose analysis is not part of this discussion.
Diagnosis
Assessment of diabetic foot ulcers includes identifying risk factors such as diabetic peripheral neuropathy, noting that 50 percent of people show no symptoms, and rule out other causes of peripheral neuropathy such as alcohol abuse and spinal cord injury.
The location of the ulcer, its size, shape, depth and whether its tissue is granulated or needs to be skinned. Further considerations include whether there is a lack, border conditions of the wound and bone are palpable and sinus formation should be investigated. Signs of infection need to be considered such as the development of gray or yellow tissue, purulent fluid, unpleasant odors, sinuses, damaged edges and bone or tendon exposure.
The identification of diabetic foot in medical databases, such as commercial claims and prescription data, is complicated by the lack of ICD-9 codes specific to diabetic feet and variations in coding practice. The following code shows the ulcer on the lower extremities or legs:
- 707.1 Ulcers in the lower extremities, except for the ulcer press
- 707.14 Heel and middle leg ulcers
- 707.15 Ulcers on other parts of the foot
- 707.19 Ulcer at the bottom of the lower limb
One or more codes, in combination with current or previous diabetes diagnosis may be sufficient to infer diabetic feet:
- 250.0 Diabetes Mellitus
- 250.8 Diabetes with other special manifestations
Prevention
Measures to prevent diabetic foot ulcers include frequent review by foot specialists, good foot cleanliness, socks and diabetic shoes, and avoid injury.
- Foot care education combined with increased surveillance can reduce the incidence of serious foot lesions.
Footwear
Proof for special footwear to prevent leg ulcers is bad.
Clinical Evidence reviewing topics and concluding "Individuals with significant foot deformities should be considered for referrals and ratings for special shoes that can accommodate altered leg anatomy.In the absence of significant abnormalities, high quality is also unsuitable Formed footwear seems to be a reasonable choice ". The National Institute for Health and Clinical Excellence concluded that for people with "high-risk foot ulcers (neuropathy or no pulse plus deformity or previous skin changes or ulcers" that "special shoes and soles" should be provided.
People who lose feelings in their feet should check their feet every day, to ensure that no injuries begin to develop. They should not walk barefoot, but use the right footwear all the time.
Treatment
Foot ulcers in diabetes require multidisciplinary assessment, usually by diabetes nurse specialists, tissue viability nurses, podiatrists, diabetes specialists and surgeons. A goal to improve glycemic control, if poor, is part of management, to slow the progression of the disease. Individuals with sausage-shaped fingers, positive probe to bone tests, evidence showing osteomyelitis, suspected neuroarthropathy charcot, or those whose ulcer did not improve within 4 weeks of standard care and where there is evidence that exudate is a synovial membrane at the origin.. When osteomyelitis is suspected of involvement in foot ulcers, but not proven on x-rays, an MRI scan should be performed.
With regard to infected foot ulcers, the presence of microorganisms is not sufficient to determine if there is infection. Signs such as inflammation and purulence are the best indicators of active infection. The most common organism causing infection is staphylococcus. Treatment consists of proper debridement, bandages, peripheral arterial disease management and appropriate antibiotic use (against pseudomonas aeruginosa, staphylococcus, streptococcus and anaerobic strains), and arterial revascularization.
Antibiotics
The duration of an antibiotic program depends on the severity of the infection and whether bone infection is involved but can range from 1 week to 6 weeks or more. The current recommendation is that antibiotics are used only when there is evidence of infection and continue until there is evidence that the infection has disappeared, not evidence of ulcer healing. The choice of antibiotics depends on a common local bacterial strain known to infect the ulcer. Microbiological swabs are believed to have limited value in identifying the causal strains. Microbiological investigations are valuable in cases of osteomyelitis. Most ulcer infections involve multiple microorganisms.
Dressing wound
There are many types of dressings used to treat diabetic foot ulcers such as absorption fillers, hydrogel dressings, and hydrocolloids. There is no good evidence that one type of sauce is better than the other for diabetic foot ulcers. In choosing a dressing for chronic healing wounds, it is recommended that product costs be taken into account.
Hydrogel dressing may have shown little benefit over standard dressing, but the quality of the research is of concern. Dressings and creams containing silver have not been studied properly or have alginate dressings. An active biologic band combining the properties of hydrogels and hydrocolloids is available, but further research needs to be done for the efficacy of this option over the others.
Checking total contact
Total contact casting (TCC) is a specially designed cast designed to take off-loading in patients with DFUs. Reducing the pressure on the wound by taking foot weight has proven to be very effective in the treatment of DFU. DFU is a major factor causing lower leg amputation among the diabetic population in the US with 85% amputation in diabetics preceded by DFU. Furthermore, the 5-year post-amputation mortality rate among diabetics is estimated at about 45% for those with neuropathic DFUs.
TCC has been used for off-loading DFUs in the US since the mid-1960s and is considered by many practitioners a "reference standard" for not loading the bottom surface (foot).
TCC helps patients to maintain their quality of life. By wrapping the patient's full legs - including the toes and lower legs - in specialist cast to distribute weight and pressure from foot to foot under daily movement, the patient can keep moving. The way in which the TCC redistributes the pressure of protecting the wound, letting the damaged tissue regenerate and heal. TCC also keeps the ankles from spinning while walking, which helps prevent shear and twisting forces that can further damage the wound.
Effective off-loading is a key treatment modality for DFU, especially where there is damage to the nerves in the leg (peripheral neuropathy). Along with infectious management and vascular assessment, TCC is an important aspect for managing DFU effectively. TCC is the most effective and reliable method for DFU that is not loaded.
A 2013 meta-analysis by Cochrane Collaboration compares the effectiveness of irreversible release-release interventions, such as plaster, with therapeutic shoes, dressings, removable pressure relievers, and surgical interventions. Non-removable pressure reliefieving, including a non-removable cast with an Achilles tendon elongation component, is found to be more effective for curing diabetic foot ulcers that shoe therapy and other pressure-relieving approaches.
Hyperbaric Oxygen
In 2015, Cochrane's review concluded that for diabetic foot ulcers, hyperbaric oxygen therapy reduces the risk of amputation and can improve healing at 6 weeks. However, there is no benefit in one year and the quality of the reviewed trials is inadequate to draw strong conclusions.
Negative pressure wound therapy
This treatment uses a vacuum to remove excess fluids and cellular waste which typically extend the inflammatory phase of wound healing. Despite the mechanism of direct action, the results of the negative pressure pressure therapy study were inconsistent. Research needs to be done to optimize the parameters of pressure intensity, maintenance interval and the right time to start negative pressure therapy in the chronic wound healing process.
Other treatments
Ozone therapy - there is only limited and poor quality information available on the effectiveness of ozone therapy to treat leg ulcers in diabetics.
Growth factors - there is some low-quality evidence that growth factors can increase the likelihood that diabetic foot ulcers will heal completely.
Epidemiology
About 15 percent of diabetics have leg ulcers. And about 84 percent of limb amputations have a history of ulceration with only about half of the amputations persisting for more than 2 years. 56 percent of individuals with leg ulcers who did not have an amputation lasted for 5 years. Foot ulcers and amputations significantly reduce quality of life. Approximately 8.8 percent of inpatients in hospital-treated hospitals are for foot-related problems, and hospital admissions are about 13 days longer than for diabetics without foot-related treatments. Approximately 35 to 40 percent of ulcers recur within 3 years and up to 70 percent recurrence within 5 years. Diabetic foot disease is a major cause of non-traumatic lower extremity amputation.
Research
Stem cell therapy may represent treatment to promote the healing of diabetic foot ulcers. Diabetic foot ulcers develop their own unique microbiota. Investigations in characterizing and identifying the phyla, genus and species of non-pathogenic bacteria or other microorganisms that feed these ulcers can help identify a group of microbiota that encourages healing.
Recent advances in epigenetic modification, with a particular focus on the polarization of aberrant macrophages are providing increasing evidence that epigenetic modification may play an important role in changing the treatment of diabetic foot ulcers in the near future.
References
External links
Source of the article : Wikipedia
0 Comments