UMLS:C0022116 - FACTA Search

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic foot infections, a common source of morbidity and mortality, often have been related to vasculopathy and neuropathy in its etiopathogenesis, especially in the elderly person with diabetes. However, blood flow in the neuropathic diabetic foot has not been evaluated extensively, and there is evidence of abnormal blood flow patterns in the neuropathic diabetic foot unrelated to ischemia. The authors studied young persons with diabetes, with varying degrees of neuropathy, to assess the extent of vasculopathy in their lower limbs. Twelve young persons with insulin-dependent (Type I) diabetes (mean age, 36.1 +/- 1.975 years) and peripheral neuropathy, all of whom had previous surgery for diabetic foot infections, were identified. Confirmatory evidence of neuropathy was made using electromyographic studies and clinical tests that showed severe peripheral neuropathy. The results of vascular assessment of both lower limbs did not reveal any change in the pulse wave velocities from the popliteal to the digital vessels of the big toe as compared with correspondingly matched controls. There also was no significant stenosis in any of the vessels studied as far as the level of the dorsalis pedis and posterior tibial vessels. The normal triphasic pattern of arterial blood flow was lost. A monophasic pattern was present in all patients with prolonged diastolic flow at the level of the dorsalis pedis and posterior tibial arteries and distally. The pulsatility index was 3.14 +/- 0.81 as compared with 9.85 +/- 4.2. Mean toe pressures in the patient with diabetes was 64.17 +/- 20.87 mm Hg as compared with 98.23 +/- 10.12 mm Hg in controls. A linear correlation of decreasing toe pressures with increasing severity of neuropathy was seen (R = 0.7). The data suggest that changes exist in the blood flow patterns in young patients with diabetes and neuropathy, even in the absence of lower limb ischemia.
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PMID:Vascular assessment in the neuropathic diabetic foot. 758 48

Lower-extremity ulcers occur in approximately 15% of the estimated 16 million Americans with diabetes. The most important risk factors are neuropathy, ischemia, and poor glycemic control. Early identification of the patient at risk, patient education, and implementation of preventive measures are keys to curtailing morbidity and mortality. Diabetic foot care clinics allow enhanced patient accessibility to health care and improved quality of care. Novel treatment options have expanded the alternatives available to clinicians treating these difficult and prevalent wounds.
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PMID:The management of lower-extremity diabetic ulcers. 1118 37

Diabetic foot wounds are difficult to manage due to relative tissue ischemia and high rates of soft tissue infection. One potential treatment modality is the application of local radiant heat to promote wound healing and control infection. However, there are concerns that local heat will spread rather than control infection. We determined in this study the effect of a noncontact radiant heat bandage in controlling an ischemic soft tissue infection. Bilateral 10 x 15 cm dermal flaps were created in 15 adult range sheep. The flaps were inoculated intradermally with 107 Staphylococcus aureus in 3 separate areas. The control flap was left open to air, while the treatment flap was covered with a noncontact radiant heat bandage and heated to 38 degrees C for three 1-hour periods separated by two 1-hour nonheating periods daily. After 10 days, both dermal flaps were harvested and sent for quantitative bacteriology. Due to operative complications, 12 of 15 sheep completed the study. The heated flap temperature was significantly higher 39.2 +/- 0.5 degrees C (+/- SE) vs. the control flap 36.1 +/- 0.1 degrees C (p < 0.00001) and bacterial counts were significantly smaller in the heated flap (median 1.0 x 107 colony-forming units per gm tissue) when compared to the control flap (median 7.5 x 107) (p = 0.001). This study shows the use of a noncontact radiant heat bandage controls ischemic soft tissue infections in an ovine model.
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PMID:Use of a noncontact radiant heat bandage and Staphylococcus aureus dermal infections in an ovine model. 1120 84

Diabetic foot wounds affect an estimated 15% of all patients with diabetes. These wounds are typically multifactorial in origin. Neuropathy of the foot and impaired wound healing are frequently associated with peripheral arterial occlusive disease. These factors combine to contribute to the development of foot ulcers. Successful wound healing and limb salvage require prompt recognition and treatment. Assessment of arterial perfusion is imperative and may be accomplished by a combination of physical examination and noninvasive vascular laboratory studies. When associated with significant ischemia, diabetic foot ulcers require arterial revascularization to achieve wound healing.
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PMID:The role of surgical revascularization in the management of diabetic foot wounds. 1514 90

Diabetic foot ulcers are frequently complicated by the presence of arterial occlusive disease (PAD). It is often difficult to assess the severity of ischemia by history and physical examination alone; a combination of different types of noninvasive laboratory testing may be necessary. Pulse-volume recordings and segmental pressures should be routinely obtained. If questions persist, an anatomic study is warranted. Duplex ultrasonography can provide accurate information with little risk to the patient and so should be readily obtained.
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PMID:Detailed protocol of ischemia and the use of noninvasive vascular laboratory testing in diabetic foot ulcers. 1514 96

Diabetic foot is one of challenging diseases in vascular surgery. This is based on uncontrolled diabetes mellitus and its true character is the neuropathic gangrene due to microangiopathy. Diabetic foot, however, is sometimes accompanied by peripheral arterial occlusive disease, which true status is macroangiopathy. Therefore, the strategy for diabetic foot is as follows;the first step is the infection control by minor amputation and/or drainage, the second step is the assessment of the limb ischemia, and the final is the complete vascular reconstruction. To salvage these diabetic feet, it is important that doctors, who concern to diabetics, understand these strategies and also that they have a settled opinion for the diabetic foot.
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PMID:[Surgical management of the diabetic foot]. 1577

The pathophysiological mechanisms underlying a diabetic foot disease are complex and multifactorial, including neuropathy, ischemia, infection and abnormal foot biomechanics. All these factors are often intricated and source of delayed wound healing. Insight in the pathophysiology of the diabetic foot provides a comprehensive basis for a protocol of primary and secondary preventive care. Since non-enzymatic glycosilation of proteins and of connective tissue underlies structural changes in vessels, nerves and osteo-articular structures, a rigid control of blood glucose levels is of paramount importance. Early recognition of the etiology of foot lesions and prompt management of foot ulcers are essential for successful outcome. Aggressive treatment of infections, clinical assessment and correction of vascular occlusive disease (diabetic macroangiopathy), adequate wound care and appropriate off-loading (pressure relief) of the ulcer are essential steps in the treatment protocol. It is not surprising that optimal management of the diabetic foot requires a multidisciplinary approach in a Diabetic Foot Clinic, coordinating care-provisions by a team of diabetologist, infectiologist, vascular surgeon, interventional radiologist, plastic surgeon, podiatrist and specialized nurse. Applying evidence-based multidisciplinary treatment results in a 50% reduction of major lower-limb amputation in this high risk group.
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PMID:[The diabetic foot]. 1603 20

Diabetic foot is caused by microangiopathy and is suggested to be a result of impaired angiogenesis. Using a severe hindlimb ischemia model of streptozotocin-induced diabetic mice (STZ-DM), we show that diabetic foot is a disease solely of the disturbance of platelet-derived growth factor B-chain homodimer (PDGF-BB) expression but not responses of angiogenic factors. STZ-DM mice frequently lost their hindlimbs after induced ischemia, whereas non-DM mice did not. Screening of angiogenesis-related factors revealed that only the expression of PDGF-BB was impaired in the STZ-DM mice on baseline, as well as over a time course after limb ischemia. Supplementation of the PDGF-B gene resulted in the prevention of autoamputation, and, furthermore, a protein kinase C (PKC) inhibitor restored the PDGF-BB expression and also resulted in complete rescue of the limbs of the STZ-DM mice. Inhibition of overproduction of advanced-glycation end product resulted in dephosphorylation of PKC-alpha and restored expression of PDGF-BB irrespective of blood sugar and HbA1c, indicating that advanced-glycation end product is an essential regulator for PKC/PDGF-BB in diabetic state. These findings are clear evidence indicating that diabetic vascular complications are caused by impairment of the PKC/PDGF-B axis, but not by the impaired expression of angiogenic factors, and possibly imply the molecular target of diabetic foot.
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PMID:Diabetic microangiopathy in ischemic limb is a disease of disturbance of the platelet-derived growth factor-BB/protein kinase C axis but not of impaired expression of angiogenic factors. 1639 50

Wound healing during the diabetic foot disease is indicated to in-patient treatment in case of non-healing wound, in case of serious infection and/or critical ischemia and in case of necessity of surgical treatment. Diabetic foot disease is the main reason for in-patient treatment of people with diabetes, which our experience confirms. Chronic wound is characterised by non-healing for at least 4 weeks. Ischemia and recurrent trauma caused by incomplete off-loading, prolong inflammation and infection are the main reasons for difficult healing of chronic wound. Infection is also leading cause for prolonged hospitalisation of patients with diabetic foot disease. Local decrease of grow factors and increase of tissue protease are characteristics of chronic wound. The process of wound healing is characterized by a cascade of interrelated events involving infection and inflammatory factors. The results of these investigations led to the moist wound healing concept and use of growth factors and bioengineered skin substitutes. We have good experience with the use of xenotransplant skin substitues in the treatment of diabetic foot. Off loading techniques including total contact casting, local therapy by debridement and skin substitutes had the best evidence based efficacy. We are introducing new method of the treatment of diabetic foot--VAC--vacuum assisted closure. The fundamental principle in the therapy during in-patient period, is comprehensive approach; the omitting of any of the principle of the therapy--e.g. the off-loading of the ulcers, the infection and ischemia control, may contribute to its failure.
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PMID:[Healing of skin lesions in diabetic foot syndrome during hospitalization]. 1677 Oct 90

EXECUTIVE SUMMARY: 1. Foot infections in patients with diabetes cause substantial morbidity and frequent visits to health care professionals and may lead to amputation of a lower extremity. 2. Diabetic foot infections require attention to local (foot) and systemic (metabolic) issues and coordinated management, preferably by a multidisciplinary foot-care team (A-II). The team managing these infections should include, or have ready access to, an infectious diseases specialist or a medical microbiologist (B-II). 3. The major predisposing factor to these infections is foot ulceration, which is usually related to peripheral neuropathy. Peripheral vascular disease and various immunological disturbances play a secondary role. 4. Aerobic Gram-positive cocci (especially Staphylococcus aureus) are the predominant pathogens in diabetic foot infections. Patients who have chronic wounds or who have recently received antibiotic therapy may also be infected with Gram-negative rods, and those with foot ischemia or gangrene may have obligate anaerobic pathogens. 5. Wound infections must be diagnosed clinically on the basis of local (and occasionally systemic) signs and symptoms of inflammation. Laboratory (including microbiological) investigations are of limited use for diagnosing infection, except in cases of osteomyelitis (B-II). 6. Send appropriately obtained specimens for culture before starting empirical antibiotic therapy in all cases of infection, except perhaps those that are mild and previously untreated (B-III). Tissue specimens obtained by biopsy, ulcer curettage, or aspiration are preferable to wound swab specimens (A-I). 7. Imaging studies may help diagnose or better define deep, soft-tissue purulent collections and are usually needed to detect pathological findings in bone. Plain radiography may be adequate in many cases, but MRI (in preference to isotope scanning) is more sensitive and specific, especially for detection of soft-tissue lesions (A-I). 8. Infections should be categorized by their severity on the basis of readily assessable clinical and laboratory features (B-II). Most important among these are the specific tissues involved, the adequacy of arterial perfusion, and the presence of systemic toxicity or metabolic instability. Categorization helps determine the degree of risk to the patient and the limb and, thus, the urgency and venue of management. 9. Available evidence does not support treating clinically uninfected ulcers with antibiotic therapy (D-III). Antibiotic therapy is necessary for virtually all infected wounds, but it is often insufficient without appropriate wound care. 10. Select an empirical antibiotic regimen on the basis of the severity of the infection and the likely etiologic agent(s) (B-II). Therapy aimed solely at aerobic Gram-positive cocci may be sufficient for mild-to-moderate infections in patients who have not recently received antibiotic therapy (A-II). Broad-spectrum empirical therapy is not routinely required but is indicated for severe infections, pending culture results and antibiotic susceptibility data (B-III). Take into consideration any recent antibiotic therapy and local antibiotic susceptibility data, especially the prevalence of methicillin-resistant S. aureus (MRSA) or other resistant organisms. Definitive therapy should be based on both the culture results and susceptibility data and the clinical response to the empirical regimen (C-III). 11. There is only limited evidence with which to make informed choices among the various topical, oral, and parenteral antibiotic agents. Virtually all severe and some moderate infections require parenteral therapy, at least initially (C-III). Highly bioavailable oral antibiotics can be used in most mild and in many moderate infections, including some cases of osteomyelitis (A-II). Topical therapy may be used for some mild superficial infections (B-I). 12. Continue antibiotic therapy until there is evidence that the infection has resolved but not necessarily until a wound has healed. Suggestions for the duration of antibiotic therapy are as follows: for mild infections, 12 weeks usually suffices, but some require an additional 12 weeks; for moderate and severe infections, usually 24 weeks is sufficient, depending on the structures involved, the adequacy of debridement, the type of soft-tissue wound cover, and wound vascularity (A-II); and for osteomyelitis, generally at least 46 weeks is required, but a shorter duration is sufficient if the entire infected bone is removed, and probably a longer duration is needed if infected bone remains (B-II). 13. If an infection in a clinically stable patient fails to respond to 1 antibiotic courses, consider discontinuing all antimicrobials and, after a few days, obtaining optimal culture specimens (C-III). 14. Seek surgical consultation and, when needed, intervention for infections accompanied by a deep abscess, extensive bone or joint involvement, crepitus, substantial necrosis or gangrene, or necrotizing fasciitis (A-II). Evaluating the limb's arterial supply and revascularizing when indicated are particularly important. Surgeons with experience and interest in the field should be recruited by the foot-care team, if possible. 15. Providing optimal wound care, in addition to appropriate antibiotic treatment of the infection, is crucial for healing (A-I). This includes proper wound cleansing, debridement of any callus and necrotic tissue, and, especially, off-loading of pressure. There is insufficient evidence to recommend use of a specific wound dressing or any type of wound healing agents or products for infected foot wounds. 16. Patients with infected wounds require early and careful follow-up observation to ensure that the selected medical and surgical treatment regimens have been appropriate and effective (B-III). 17. Studies have not adequately defined the role of most adjunctive therapies for diabetic foot infections, but systematic reviews suggest that granulocyte colony-stimulating factors and systemic hyperbaric oxygen therapy may help prevent amputations (B-I). These treatments may be useful for severe infections or for those that have not adequately responded to therapy, despite correcting for all amenable local and systemic adverse factors. 18. Spread of infection to bone (osteitis or osteomyelitis) may be difficult to distinguish from noninfectious osteoarthropathy. Clinical examination and imaging tests may suffice, but bone biopsy is valuable for establishing the diagnosis of osteomyelitis, for defining the pathogenic organism(s), and for determining the antibiotic susceptibilities of such organisms (B-II). 19. Although this field has matured, further research is much needed. The committee especially recommends that adequately powered prospective studies be undertaken to elucidate and validate systems for classifying infection, diagnosing osteomyelitis, defining optimal antibiotic regimens in various situations, and clarifying the role of surgery in treating osteomyelitis (A-III).
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PMID:Diagnosis and treatment of diabetic foot infections. 1547 38

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