Diabetic foot ulcer
Diabetic foot ulcer | |
---|---|
Neuropathic diabetic foot ulcer | |
Causes | diabetes |
Diabetic foot ulcer is a breakdown of the skin and sometimes deeper tissues of the foot that leads to sore formation. It may occur due to a variety of mechanisms. It is thought to occur due to abnormal pressure or mechanical stress chronically applied to the foot, usually with concomitant predisposing conditions such as
Treatment of diabetic foot ulcers should include:
It occurs in 34% of people with diabetes during their lifetimes, and it is associated with a high morbidity and mortality with 84% of all diabetes-related lower-leg
Risk factors
Risk factors implicated in the development of diabetic foot ulcers are infection, older age,
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, feet, legs, and arms due to distal nerve damage and low blood flow. Autonomic neuropathy causes Sudomotor dysfunction and dryness of the skin. Blisters and sores may appear on numb areas of the feet and legs, such as metatarsophalangeal joints and the heel region, as a result of pressure or injury which may go unnoticed and eventually become a portal of entry for bacteria and infection.[citation needed]
Pathophysiology
Extracellular matrix
Through the interaction of a cell with its
The cells break down damaged
In the initial events of wound healing,
The basement membrane that separates the epidermis from the dermal layer and the endothelial basement membrane mainly contains collagen IV that forms a sheet and binds to other extracellular matrix molecules like laminin and proteoglycans. In addition to collagen IV, the epidermal and endothelial basement membrane also contains laminin, perlecan and nidogen.
Altered metabolism
- Impaired NO synthesis
- differentiation. Thus, nitric oxide increases fibroblast proliferation and thereby collagen production in wound healing. Also, L-arginine and nitric oxide are required for proper cross linking of collagen fibers, via proline, to minimize scarring and maximize the tensile strength of healed tissue.[21] Endothelial cell specific nitric oxide synthase (EcNOS) is activated by the pulsatile flow of blood through vessels. Nitric oxide produced by EcNOS, maintains the diameter of blood vessels and proper blood flow to tissues. In addition to this, nitric oxide also regulates angiogenesis, which plays a major role in wound healing.[22] Thus, diabetic patients exhibit reduced ability to generate nitric oxide from L-arginine. Reasons that have been postulated in the literature include accumulation of nitric oxide synthase inhibitor due to high glucose associated kidney dysfunction and reduced production of nitric oxide synthase due to ketoacidosis observed in diabetic patients and pH dependent nature of nitric oxide synthase.[18][23]
- Structural and functional changes in fibroblasts
- Diabetic ulcer microtubules to release the products outside.[24][25] Fibroblasts from diabetic ulcer exhibit proliferative impairment that probably contributes to a decreased production of extracellular matrix proteins and delayed wound contraction and impaired wound healing.[24]
- Increased matrix metalloproteinases (MMP) activity
- In order for a wound to heal, cytokines. To mention precisely, growth factors promote switching of early inflammatory phase to the granulation tissue formation. Decrease in growth factors responsible for tissue repair such as TGF-β is documented in diabetic wounds. Thus, reduced levels of TGFβ in diabetes cases lower down the effect of inhibitory regulatory effect on MMP genes and thus cause MMPs to over express.[32][33][34]
Biomechanics
Complications in the diabetic foot and foot-ankle complex are wider and more destructive than expected and may compromise the structure and function of several systems: vascular, nervous, somatosensory, musculoskeletal. Thus, deeper comprehension of the alteration of gait and foot biomechanics in the diabetic foot is of great interest and may play a role in the design and onset of preventive as well as therapeutic actions.[citation needed]
Briefly, the effect of diabetes on the main structures of the foot-ankle complex can be summarised as:
- effects on the skin: skin – and the soft tissues immediately underneath the skin – undergo greater compression and shear loading than usual, thus explaining the onset of tissue damage so deeply correlated to traumatic ulceration processes. Besides this, skin of the diabetic foot loses autonomic nervous control and consequently reduced hydration, making it less elastic and thus more vulnerable to the action of increased mechanical stress;
- effects on tendons and ligaments: protein glycosylation and the resulting collagen abnormalities lead to greater transversal section – i.e. thickening – of tendons and ligaments and a greater coefficient of elasticity. Particularly affected by this process are Plantar Fascia and Achilles Tendon. Both causes lead to increased stiffness of those structures;
- effects on cartilage: similar to what happens to tendons and ligaments, cartilage changes its composition mainly due to the modification of collagen fibers. This increases its stiffness and decreases the range of motion of all joints in the foot and ankle.
- effects on muscles: Diabetes mellitus causes severe damage to nerve conduction, thus causing a worsening in the management of the related muscle fibers. As a consequence, both intrinsic and extrinsic muscles of the foot-ankle complex are damaged in structure (reduction of muscle volume) and function (reduction of muscle strength);
- effects on the peripheral sensory system: impaired nerve conduction has a dramatic effect on the peripheral sensory system since it leads to loss of protective sensation under the sole of the foot. This exposes the diabetic foot to thermal or mechanical trauma, and to the late detection of infection processes or tissue breakdown;
- effects on foot morphology (deformities): due to most of the above alterations, a significant imbalance of peripheral musculature and soft tissue occur in the foot which seriously alters its morphology and determines the onset of foot deformities. Most common deformities of the diabetic foot are represented by a high longitudinal arch (rigid cavus foot), hammer toes and hallux valgus. A completely different morphologic degeneration is represented by neuropathic arthropathy, whose analysis is not part of this discussion.[35][36][37][38][39]
Diagnosis
Assessment of diabetic foot ulcer includes identifying risk factors such as diabetic peripheral neuropathy, noting that 50 percent of people are asymptomatic, and ruling out other causes of peripheral neuropathy such as
The location of the ulcer, its size, shape, depth and whether the tissue is granulating or sloughy needs to be considered. Further considerations include whether there is
Classification
Diabetic foot ulcer is a complication of diabetes. Diabetic foot ulcers are classified as either
Doctors also use the Wagner Grades to describe the severity of an ulcer. The purpose of the Wagner Grades is to allow specialists to better monitor and treat diabetic foot ulcers. This grading system classifies Diabetic foot ulcers using numbers, from 0 to 5.
Wagner Grades 0 through 5 are as follows:[citation needed]
- 0. No diabetic foot ulcer is present, but there is a high risk of developing one.
- 1. A surface ulcer involves full skin thickness, but does not yet involve the underlying tissues.
- 2. A deep ulcer penetrates past the surface, down to the ligaments and muscle. There is no abscess or bone involved yet.
- 3. A deep ulcer occurs with inflammation of subcutaneous connective tissue or an abscess. This can include infections in the muscle, tendon, joint, and/or bone.
- 4. The tissue around the area of the ulcer (limited to the toes and forefoot) has begun to decay. This condition is called gangrene.
- 5. Gangrene has spread from the localized area of the ulcer to become extensive. This involves the whole foot.
Prevention
Steps to prevent diabetic foot ulcers include frequent review by a
There is no high quality researches that evaluate complex intervention of combining two or more preventive strategies in preventing diabetic foot ulcer.[46]
Monitoring and prediction
People with loss of feeling in their feet should inspect their feet on a daily basis, to ensure that there are no wounds starting to develop.[47][48] Monitoring a person's feet can help in predicting the likelihood of developing ulcers.[citation needed]
A common method for this is using a special thermometer to look for spots on the foot that have higher temperature which indicate the possibility of an ulcer developing.[49] At the same time there is no strong scientific evidence supporting the effectiveness of at-home foot temperature monitoring.[50]
The current guideline in the United Kingdom recommends collecting 8-10 pieces of information for predicting the development of foot ulcers.[51] A simpler method proposed by researchers provides a more detailed risk score based on three pieces of information (insensitivity, foot pulse, previous history of ulcers or amputation). This method is not meant to replace people regularly checking their own feet but complement it.[49][52]
Footwear
Diabetic shoes, insoles and socks are personalised products that relieve pressure on the foot in order to prevent ulcers.[53] The evidence for special footwear to treat foot ulcers is poor[54] but their effectiveness for prevention is well-established.[55][56][57] Design features of footwear that are effective in reducing pressure are arch supports, cushioned cut-outs around points at risk of damage, and cushioning at the ball of the foot. Technology for measuring the pressure within the shoes is recommended during designing diabetic footwear.[58][59]
People with loss of feeling in their feet should not walk around barefoot, but use proper footwear at all times.
Treatment
Foot ulcers in diabetes require a multidisciplinary team that may include the primary care doctor, a diabetes nurse specialist, a tissue viability nurse,
With regards to infected foot ulcers, the presence of microorganisms is not in itself enough to determine whether an infection is present. Signs of an infection such as erythema,
Antibiotics
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.[6] Microbiological investigation is of value in cases of osteomyelitis.[42] Most ulcer infections involve multiple microorganisms.[5]
There is limited safety and efficacy data of topical antibiotics in treating diabetic foot ulcers.[60]
Wound dressings
There are many types of dressings used to treat diabetic foot ulcers such as absorptive fillers, hydrogel dressings, and hydrocolloids.[61] There is no good evidence that one type of dressing is better than another for diabetic foot ulcers.[62] In selecting dressings for chronic non healing wounds it is recommended that the cost of the product be taken into account.[63]
Hydrogel dressings may have shown a slight advantage over standard dressings, but the quality of the research is of concern.[64][65] Dressings and creams containing silver have not been properly studied[66] nor have alginate dressings.[67] 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.[61]
Total contact casting
Total contact casting (TCC) is a specially designed cast designed to take weight of the foot (off-loading) in patients with DFUs. Reducing pressure on the wound by taking weight of the foot has proven to be very effective in DFU treatment. DFUs are a major factor leading to lower leg amputations among the diabetic population in the US with 85% of amputations in diabetics being preceded by a DFU.[68] Furthermore, the 5 year post-amputation mortality rate among diabetics is estimated at 45% for those with neuropathic DFUs.[68]
TCC has been used for off-loading DFUs in the US since the mid-1960s and is regarded by many practitioners as the "reference standard" for off-loading the bottom surface (sole) of the foot.[69]
TCC helps patients to maintain their quality of life. By encasing the patient's complete foot — including the toes and lower leg — in a specialist cast to redistribute weight and pressure from the foot to the lower leg during everyday movements, patients can remain mobile.[70] The manner in which TCC redistributes pressure protects the wound, letting damaged tissue regenerate and heal.[71] TCC also keeps the ankle from rotating during walking, which helps prevent shearing and twisting forces that can further damage the wound.[72]
Effective off loading is a key treatment modality for DFUs, particularly those where there is damage to the nerves in the feet (peripheral neuropathy). Along with infection management and vascular assessment, TCC is vital aspect to effectively managing DFUs.[72] TCC is the most effective and reliable method for off-loading DFUs.[73][74][75]
A 2013
TCC systems include TCC-EZ (Integra LifeSciences) and Cutimed Off-loader (BSN Medical).[77]
Hyperbaric oxygen
In 2015, a
Negative pressure wound therapy
This treatment uses
There is low-certainty evidence that negative pressure wound therapy would improve wound healing in diabetic foot ulcers.[80]
Other treatments
Ozone therapy – there is only limited and poor-quality information available regarding the effectiveness of ozone therapy for treating foot ulcers in people with diabetes.[81]
Continuous diffusion of oxygen (CDO) - CDO delivers continuous oxygen to an occluded, moist wound site at much lower flow rates of 3–12 mL/h for 24 h 7 days a week for up to several weeks or months, depending on the wound status.[83]
Sucrose-octasulfate impregnated dressing is recommended by the International Working Group on the Diabetic Foot Ulcer (IWGDF)[85] for the treatment of non-infected, neuro-ischaemic diabetic foot ulcers that do not show an improvement with a standard of care regimen[86]
Autologous combined leucocyte, platelet and fibrin as an adjunctive treatment, in addition to best standard of care is also recommended by IWGDF[87] However, there is only low quality evidence that such treatment is effective in treating diabetic foot ulcer.[88]
There is limited evidence that granulocyte colony-stimulating factor may not hasten the resolution of diabetic foot ulcer infection. However, it may reduce the need for surgical interventions such as amputations and hospitalizations.[89]
It is unknown that whether intensive or conventional blood glucose control is better for diabetic foot ulcer healing.[90]
A 2020 Cochrane systematic review evaluated the effects of nutritional supplements or special diets on healing foot ulcers in people with diabetes. The review authors concluded that it's uncertain whether or not nutritional interventions have an effect on foot ulcer healing and that more research is needed to answer this question.[91]
Skin grafting and tissue replacements can help to improve the healing of diabetic foot ulcer.[92]
A 2021 systematic review concluded that there was no strong evidence about the effects of psychological therapies on diabetic foot ulcer healing and recurrence.[93]
Epidemiology
Approximately 34% of people with diabetes (Type 1 or Type 2 diabetes) will develop a foot ulcer in their lifetime.[1] 18.6 million people worldwide will develop a foot ulcer each year.[1] 15-20% of moderately to severely infected foot ulcers eventually lead to amputation, and the mortality rate of diabetic foot ulcers is 30% at 5 years with a mortality rate of 70% in those with a foot ulcer who receive an above the foot amputation.[1] Foot ulcers and amputations are associated with a reduced quality of life. In the United States; Black people, Native Americans, Hispanics and those living in rural areas or those with a lower socioeconomic status have an increased rate of amputations due to diabetic foot ulcers.[1]
Approximately 8.8 percent of hospital admissions of diabetic patients are for foot related problems, and such hospital admissions are about 13 days longer than for diabetics without foot related admissions.[5] Approximately 58% of ulcers recur within 3 years and up to 65% recur within 5 years, sometimes at a different location that the original ulcer.[79] Diabetic foot disease is the leading cause of non-traumatic lower limb amputations.[6]
Research
Stem cell therapy may represent a treatment for promoting healing of diabetic foot ulcers.
The recent advances in epigenetic modifications, with special focus on aberrant macrophage polarisation is giving increasing evidences that epigenetic modifications might play a vital role in changing the treatment of diabetic foot ulcer in the near future.[97]
References
- ^ S2CID 259314584.
- ^ Nomikos Iakovos N, et al. (2006). "Protective and Damaging Aspects of Healing: A Review". Wounds. 18 (7): 177–185.
- ^ a b c McLennan S, et al. (2006). "Molecular aspects of wound healing" (PDF). Primary Intention. 14 (1): 8–13. Archived from the original (PDF) on 2010-05-24. Retrieved 2009-05-28.
- ^ PMID 25685277.
- ^ PMID 24796080.
- ^ PMID 23123487.
- ^ ISSN 1357-3039.
- S2CID 72816348.
- PMID 17583176.
- ISBN 978-0-306-40785-7.
- S2CID 34904588.
- ^ Schultz GS, Ludwig G, Wysocki A (2005). "Extracellular matrix: review of its roles in acute and chronic wounds". World Wide Wounds.
- ^ ISBN 978-0-7817-7444-4.
- ^ PMID 7699500.
- ^ PMID 9804349.
- ^ US 7141551, Decarlo AA, Whitelock J, "Wound and cutaneous injury healing with a nucleic acid encoding perlecan.", published 28 November 2006
- ^ Close-Tweedie J (June 2002). "Diabetic foot wounds and wound healing: a review". The Diabetic Foot. 5 (2): 68–76.
- ^ PMID 16894049.
- PMID 11270668.
- S2CID 16119897.
- PMID 16171977.
- PMID 15162796.
- PMID 18256374.
- ^ S2CID 25658536.
- PMID 849809.
- ^ PMID 10998429.
- PMID 10414498.
- PMID 8392530.
- PMID 12136400.
- PMID 18387077.
- PMID 10997695.
- PMID 17476353.
- PMID 8392302.
- S2CID 20859528.
- PMID 19341560.
- S2CID 24862107.
- S2CID 34029708.
- PMID 18442178.
- ISBN 978-0-8493-3971-4.
- PMID 34713964.
- S2CID 46766290.
- ^ PMID 21841646.
- ^ Hamilton R, Hamilton J. "Diabetic Ulcers: Everything You Need to Know". Healing Your Wound. Retrieved September 6, 2018.
- ^ "Diabetic Socks - What is a Diabetic Sock & What Socks are Available". Diabetes.co.uk. 2019-01-15.
- S2CID 35492751.
- PMID 26299991.
- ^ "Foot Care". American Diabetes Association. Archived from the original on 2015-07-07. Retrieved 2015-08-04.
- ^ "Amputation and diabetes: How to protect your feet". Mayo Clinic.
- ^ S2CID 251787297.
- S2CID 251981184.
- ^ "Diabetic foot problems: prevention and management". National Institute for Health and Care Excellence (NICE). 26 August 2015. Retrieved 2022-09-06.
- PMID 34035053.
- S2CID 251299176.
- PMID 25245020.
- S2CID 24862853.
- S2CID 12012686.
- S2CID 210830578.
- PMID 33532602.
- S2CID 241787869.
- PMID 28613416.
- ^ PMID 15306987.
- PMID 26171906.
- PMID 23740766.
- PMID 23846869.
- PMID 20091547.
- PMID 16437516.
- PMID 23799857.
- ^ PMID 22049565.
- PMID 15306986.
- PMID 18579926.
- PMID 25694793.
- ^ PMID 25514266.
- PMID 11375363.
- S2CID 24007485.
- PMID 23440787.
- PMID 23440787.
- S2CID 208230168.
- ^ PMID 26106870.
- ^ PMID 11993062.
- PMID 30328611.
- PMID 26505864.
- PMID 26509249.
- S2CID 258699243.
- ^ PMID 28657134.
- ^ "Wound healing interventions guideline". IWGDF Guidelines. 2019-05-25. Retrieved 2020-05-15.
- PMID 29275068.
- S2CID 52341731.
- PMID 27223580.
- PMID 23955465.
- PMID 26758576.
- PMID 32677037.
- PMID 26866804.
- PMID 35653236.
- PMID 22142631.
- PMID 21234108.
- PMID 25566413.
- PMID 29530315.
97.^ Jayesh Kakar https://savelegs.com/negative-pressure-wound-therapy-in-foot-infections-in-diabetics-effect-on-duration-of-antibiotic-therapy-method-negative-pressure-wound-therapy-has-be/External links