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Hyperosmolar hyperglycemic state is a relatively common, life-threatening endocrine emergency that is reported in all age groups,1 but it most frequently affects older patients with type 2 diabetes.2 The hallmark of hyperosmolar hyperglycemic state is profound dehydration, marked hyperglycemia, and often some degree of neurologic impairment with mild or no ketosis. Influence of age on the presentation and outcome of acidotic and hyperosmolar diabetic emergencies.
Diabetic ketoacidosis and hyperosmolar nonketotic state: gaining control over extreme hyperglycemic complications. Clinical characteristics and outcome of hyperglycaemic emergencies in Johannesburg Africans. Hyperosmolar non-ketotic diabetic coma as a cause of emergency hyperglycaemic admission to Baragwanath Hospital.
A case of hyperosmolar nonketotic coma occurring during chemotherapy using cisplatin for gallbladder cancer.
Hyperosmolar nonketotic diabetic syndrome following treatment of human immunodeficiency virus infection with didanosine.
Hyperosmolar hyperglycaemic nonketotic coma associated with acute myocardial infarction: report of three cases.
Cushing’s syndrome manifesting as pseudocentral hypothyroidism and hyperosmolar diabetic coma. The Journal of Diabetic Foot Complications The Journal of Diabetic Foot Complications, 2012; Volume 4, Issue 2, No. Diabetes mellitus (DM) is a global epidemic, and diabetic foot ulcer (DFU) is one of its most serious and costly complications. Diabetic foot infection (DFI) treatment accounts for up to one-quarter of all diabetic admissions in both Europe and the United States making it the single most common reason for DM-related hospital admission 6. Recognizing this predictable progression, the solution includes developing structured screening tools to identify those at risk and implementing both standardized education and prevention protocols.
Diabetic peripheral neuropathy results from degenerative changes of axons and affects all nerve fibers, but at different times. The first notion to consider is that vascular disease of the diabetic foot always results from tight and obliterative atherosclerosis in the large limb vessels and not from, as is most commonly believed, microvascular disease 21.
Once the protective layer of skin is broken, the deep tissues are exposed to bacterial colonization 28. Staphylococcus aureus and ß-hemolytic streptococci are the first microorganisms to colonize and acutely infect breaks in the skin.
Assuming that the qualitative microbiology remains constant, the probability of wound infection increases as the microbial load increases to a critical level. All of these complex interactions have been systematized by the wound infection continuum 34.
In the acute wound setting, once the protective barrier is broken, the physiologic process of healing is immediately set in motion (Figure 3).
In this classic model 35 wound healing is divided into three sequential but overlapping phases: (1) the inflammatory phase, (2) the proliferative phase (re-epithelialization, granulation, and neo-angiogenesis), and (3) the remodeling phase (extracellular matrix remodeling).
The inflammatory phase starts with injury-related subendothelial collagen-mediated platelet activation. The proliferation phase begins at 72 hours, as recruited fibroblasts migrate inward from the wound margins over the fibrin matrix established during the inflammatory phase. Chronic wounds are wounds that, following the orderly and timely repair process, fail to establish a sustained anatomic and functional result 39. Recognizing important risk factors and making a logical treatment-oriented assessment of DFIs requires a consistent and thorough diagnostic approach.
Based on the present literature 25,44, the presence of both pulses in the foot, in combination with the absence of intermittent claudication, renders significant PAD unlikely. Although the PEDIS classification system suggests the use of toe pressures or TcPO2 to exclude clinically relevant vascular disease 44, the complexity and cost of its use precludes its generalized application outside of clinical studies.
The International Working Group on the Diabetic Foot has proposed consensus criteria 55 for diagnosing diabetic foot osteomyelitis (Table 1) that remain to be validated in a properly designed trial.
In the absence of suspected osteomyelitis, bacteriological sampling, which must be done after mechanical debridement and cleansing of the wound with gauze soaked in sterile physiological saline, is indicated if a DFI ≥ Grade 2 is clinically confirmed. Although research continues to improve wound-healing modalities and show promising options for the future, the importance of prevention cannot be overemphasized. When treating a DFI, the multidisciplinary team must consider the need for hospitalization, prioritize the treatment and drainage of any invasive infection, and perform limited debridement if necrosis is present.
When used after adequate debridement in a well-vascularized bed, NPWT prepares the wound for closure by secondary intention or skin graft. Hospitalization is the first decision to make regarding patients with a DFI, and determining its necessity requires considering many aspects. Invasive infection drainage should be the first-line treatment for all ulcers, especially those associated with abscesses complicated by compartmental syndrome, extensive necrosis, or necrotizing cellulitis. If the lesion is healing and the patient is tolerating the empirical regimen, then there may be no reason to change, even if some or all of the isolated organisms are resistant to the agents used. Other factors that must be taken into account when selecting an antibiotic regimen are the route of administration (oral vs. The presence of bone infection substantially alters the approach to therapy, but there are no validated or well-accepted guidelines for treating diabetic foot osteomyelitis 29,60. In the case of critical ischemia, once the infection has been controlled, revascularization must be immediately considered.
Drainage and debridement (surgical, mechanical, sharp, etc.) are two different but complementary surgical procedures. The presence of clotted vessels, stringy fascia, or tendon indicates that the tissue is not viable and should be removed and shaved down to shiny hard tendon or fascia. Wet-to-dry dressings, hydrotherapy, biotherapy, and other topical debriding agents provide alternative options to surgical debridement.
NPWT includes a family of devices consisting of specialized dressings, including adhesive drape and open-cell foam, cut to fill the wound defect and capable of transmitting constant or intermittent pressure throughout the wound using a feedback control mechanism. Excessive physiopathological exudate in DFIs can be detrimental because it contains an imbalance of matrix metalloproteases (MMPs) and their inhibitors (TIMPs). Several subsequent studies have demonstrated NPWT’s effectiveness in DFIs, particularly to treat osteomyelitis and soft tissue infections 65,91-93, when used in conjunction with adequate debridement and appropriate antibiotics. No intervention is likely to be successful if the wound is not protected against external trauma; therefore, complete and permanent off-loading of the wound must be ensured as strictly as possible. Diabetic Ketoacidosis (DKA) is a life-threatening emergency condition that often occurs in patients with type I Diabetes. The early stages of cancer may be asymptomatic, but a malignant tumor will eventually grow–large enough to be detected. Other symptoms include persistent headaches, chronic pain in bones and various areas of the body, persistent fatigue, persistent low-grade fever and repeated infection. Nurses are encouraged to provide as much care and comfort as possible to patients with cancer. Priorities of care include provision of information about the disease, prevention of complications, promotion of comfort and preservation of optimal physiological functioning. With the dramatic increase in the prevalence of type 2 diabetes and the aging population, this condition may be encountered more frequently by family physicians in the future.
Traditionally, hyperosmolar hyperglycemic state and diabetic ketoacidosis (the other result of severe diabetic decompensation; see the Trachtenbarg article3 on p. Glucosuria impairs the concentrating capacity of the kidney, further exacerbating water loss.
Myocardial infarction,13,16 cerebrovascular accident, pulmonary embolus, and mesenteric thrombosis have been identified as causes of hyperosmolar hyperglycemic state. They often take medications that aggravate the problem, such as a diuretic that causes mild dehydration.
While a detailed discussion of the management of hyperosmolar hyperglycemic state in children and adolescents is beyond the scope of this article, an algorithm from the ADA guideline is included in the Trachtenbarg3 article on page 1705 of this issue.
Cerebral edema should be treated with intravenous mannitol (Osmitrol) in a dose of 1 to 2 g per kg over 30 minutes and intravenous dexamethasone (Decadron). There are an estimated 171 million diabetic patients worldwide and this number is expected to double by the year 20301. In the longer term, costs are even higher as DFUs have recurrence rates of up to 70% in centers of excellence, resulting in repeated interventions and progressive disability7.
Different countries and healthcare systems have implemented such approaches to diabetic foot care, some with reported success 4 and others with reported failure 8. This is true even though, in some cases, the wound may have closed over before DFI presentation 9.Numerous observational studies have indicated that DFUs have a multifactorial nature. The non-myelinated autonomic nerve fibers are affected first, resulting in autosympathectomy with consequent medial artery calcification (Mönckeberg calcification), microvascular thermoregulatory dysfunction, and arteriovenous shunting 16.
This confusion results from the theoretical conclusion that diabetic multifactorial microvascular insufficiency applies to the foot; however, even the almost universal basal membrane thickening is not likely to be present in the foot capillaries 22.
Qualitative and quantitative aspects of wound microbiology are critical determinants of the wound outcome (Figure 2).
Chronic wounds develop a more complex polymicrobial microbiology, including aerobic Gram-negative rods and anaerobes. This concept describes the effects of increasing bacteria quantity and diversity in wound tissue, and their relationship to the quality of the host’s immune response. Wound healing is divided into three sequential but overlapping phases: (1) the inflammatory phase, (2) the proliferative phase (re-epithelialization, granulation, and neoangiogenesis), and (3) the remodeling phase (extracellular matrix remodeling). This complexly orchestrated biochemical cascade is characterized by signature events and cells, and their molecular regulators 36. Initially stimulated by bFGF and PDGF, fibroblasts begin to synthesize and deposit extracellular matrix (ECM) components (the provisional matrix). The current thinking is that imbalances exist in the molecular environment of these chronic nonhealing wounds. Although it was not developed as a guide for daily management or to predict the outcome of an individual patient, it considers all the potentially useful information obtained from the clinical history, foot examination and diagnostic exams. The presence of both pulses in the foot, in combination with the absence of intermittent claudication, renders significant PAD unlikely. On the contrary, if one or two pulses are absent, clinically relevant PAD is more likely; however, pulses can be absent because of edema, making additional objective vascular assessment necessary to exclude PAD or to grade it if it is present 46. When used in clinical practice, the formal revascularization decision is based on information from previous clinical tests and duplex ultrasonography (B mode, color flow, and spectral Doppler analysis) 48.
Loss of protective sensation in the affected foot is defined as absent light pressure sensation at two out of three sites on the plantar side of the foot (plantar aspect of hallux, first metatarsal, and fifth metatarsal), as described in the International Consensus on the Diabetic Foot 15.
The size could be evaluated using a precise technique (planimetry or grid technique), however, this is not always possible in clinical practice. These scans are more sensitive but rather nonspecific, especially in neuropathic patients 10. Bacteriological sampling is indicated if a diabetic foot infection (DFI) corresponding to PEDIS Grades ≥2 has been clinically confirmed.
However, it should be noted that many of these tests lack the ability to provide a definitive diagnosis, and clinical correlation is always required. The clinically predictable progression from DFU to DFI, present in 85% of amputation cases 63, highlights the importance of implementing an integrated, standardized prevention and treatment protocol.
The multidisciplinary team must consider draining invasive infections, debriding necrosis, and promptly starting empirical antibiotic therapy, followed by complete and appropriate vascular reconstruction.
The assessment of vascular supply adequacy as well as a complete and appropriate vascular reconstruction follows.
A wound that fails to improve within 2 to 4 weeks should prompt the clinician to consider alternative and adjunctive therapies (assuming appropriate attention to debridement, infection, ischemia, offloading, and nutritional status).
Patients with severe infection (Grade 4), deep wounds, suspected bone and joint involvement, and severe ischemia (gangrene) should be hospitalized. Randomized clinical trials have shown that systemic antibiotics (including the most recently available agents) are of clinical value in DFI 10,66 and, as in the majority of infectious diseases, they must be provided as early as possible. When culture and sensitivity results are available, these should be considered to select a narrower-spectrum antibiotic therapy and complete the course of therapy. This is well illustrated by the Sidestep study 69, in which a favorable clinical response to ertapenem was noticed in patients in whom Enteroccus spp. Classically, bone resection in chronic osteomyelitis was considered essential to a cure 60.
Ideally, revascularization should be done at the same time as the formal debridement procedure. Soft, grey bone is necrotic and should be resected to reveal clean, hard bone with punctuated bleeding at the surface. Unfortunately, they are less definitive and controllable, require prolonged and repeated applications, and delay the application of other therapies 82. NPWT has proven its effectiveness in various diabetic foot wounds in several randomized, controlled studies 83-85; however, most of these studies have not addressed the preoperative infectious status, and few have addressed the use of NPWT in DFI. NPWT increases the diffusion gradients, which facilitates the removal of excess interstitial fluid and infectious materials and improves blood flow as well as consequent metabolic waste evacuation. A new strategy to amplify the bioburden control using a modified NPWT system with an infusion port to intermittently instill antimicrobial agents has been developed 94, but it has not been properly investigated in the clinical setting. Many types of devices can off-load the infected wound, but it is important to choose one that permits easy inspection.
It occurs when the sugar (glucose) in your body is not enough to be used as fuel for cells. The more it grows, the more it presses on nerves, producing pain and interfering with bodily functions.
Interventions (CANCER) should be focused on patient’s comfort, altered body image, nutrition, chemotherapy, response to medications and respite for caretakers.
It gets complicated at the worst of times, and sometimes you have no idea where to go or what to do. Under normal conditions, the kidneys act as a safety valve to eliminate glucose above a certain threshold and prevent further accumulation.
In one study18 of an urban population presenting with hyperosmolar hyperglycemic state, the three leading causes were poor compliance with medication, ethanol ingestion, and cocaine use. If the patient lives alone, a family member or friend should check in on the patient daily to watch for any changes in mental status and to notify the physician if this occurs. Once the protective layer of skin is broken, deep tissues are exposed to bacterial infection that progresses rapidly. It is well established that insulin deficiency (absolute or relative) is the basis of the biochemical abnormalities that lead to the organic complications of diabetes mellitus 12 (namely, neuropathy) and the biological deficits of tissue healing and regeneration. Neuropathy (with alterations in motor, sensation, and autonomic functions) plays the central role and causes ulcerations due to trauma or excessive pressure in a deformed foot without protective sensibility. Mönckeberg calcification, unlike atherosclerosis, does not reduce the arterial internal diameter.

DM is associated with a near 3-fold increased risk of accelerated atherosclerosis, which is histologically identical to that seen in the non-diabetic population 23. Chronic wounds develop a more complex polymicrobial microbiota, including aerobic Gram-negative rods and anaerobes. Gram-negative bacilli, mainly Enterobacteriaceae, are found in many patients with chronic or previously treated infections, and Pseudomonas aeruginosa is specifically associated with wounds treated with wet dressings 29. In complex extremity wounds, this critical level has been established by Breidenbach et al. This complexly orchestrated biochemical cascade is characterized by signature events and cells, and their molecular regulators.
In recent years, the scientific study of wound healing has progressed greatly making it impossible to summarize all the current knowledge in this article. This initially results in vasoconstriction and the formation of a fibrin clot, which becomes the pathway for cellular influx and the primary foundation for collagen deposition 37. ECM is composed of fibrinous elements (collagen, elastin and structural glycoproteins) and glycosaminoglycans (chondroitin sulfate, hyaluronic acid and dermatan sulfate), which attract large amounts of water and sodium collagen.
Although classically described at the end of the proliferative phase, it actually begins concurrently with the formation of the granulation tissue and continues until the tissue reaches maturation. That is, when the scales are tipped towards high levels of MMPs and proinflammatory cytokines along with senescent cells, there is a low mitogenic activity that invariably results in chronicity 40.
Various systems have been proposed to classify DFUs, but none have gained widespread acceptance.
Consequently, the use of this systematic examination ensures that important aspects are not overlooked. The ultrasonographic exam is a good, noninvasive method for delineating the peripheral arteries and enables the distinction of high-flow functional arteriopathy. The properly calibrated 10-gram monofilament is an objective and simple instrument used to screen the diabetic foot for loss of protective sensation and has shown to be a significant and independent predictor of likely lower extremity amputations in the diabetic population 50.
Instead, wound size and depth can be estimated by multiplying the largest diameter by the perpendicular largest diameter 44.
Further qualitative definitions of clinical interest should also be considered: cellulitis (infection of the subdermis), necrotizing cellulitis (infection-related tissue necrosis of the subdermis and dermis), necrotizing fasciitis (infection with involvement of the superficial fascia, presenting as sloughing of the skin and a violaceous color of the integument, without pus or abscess), wet gangrene (infection associated with blackish necrotic tissues), and osteomyelitis (infection of the bone). The initial imaging studies should be plain radiographs, as they often show characteristic pathological findings in established cases. Combining bone scans with other scintigraphic techniques, such as white blood cell scans (Indium-111 leukocyte scans or other variations), improves specificity, although these tests are rarely used because they are expensive and time consuming 59. While tissue biopsy and fluid aspirate are considered the gold standard for diagnosing wound infection 28, such invasive tests are infrequently performed for superficial wounds or in many practice settings, such as outpatient clinics, due to concerns about enlarging the ulcer or inducing pain 28,62. Mechanical debridement and wound cleansing with gauze soaked in sterile physiological saline must precede sampling. In this disease-management program, prevention strategies should be delivered by family physicians and diabetologists using structured screening tools at defined intervals, with high-risk patients referred to multidisciplinary foot care teams for treatment. A biomechanically sound surgical reconstruction, with or without amputation, must be considered part of the treatment plan to minimize the risk of recurrent ulceration. They often may require surgical intervention (debridement, drainage, bone resection, or possibly urgent revascularization), fluid resuscitation, and metabolic derangement regulation through strict glycemic control (usually using insulin therapy).
However, as authoritative guidelines emphasize 10,11 and a recent systematic review confirms 67, no particular antimicrobial regimen has been shown to be superior to others in DFI treatment. If the lesion is healing and the patient is tolerating the empirical regimen, there may be no reason to change, even if some or all of the isolated organisms are resistant to the agents used.
The parenteral route should be used for severe infections, in the neuroischemic foot, when the agents used cannot be administered orally, or when the patient’s state is incompatible with oral therapy. This routine, however, has recently been disputed 72 because radical surgical solutions (such as transmetatarsal amputations) may result in altered biomechanics, with a consequent higher risk of reulceration. In other cases, revascularization can be deferred and proposed secondarily, especially in cases of delayed healing. This surgical procedure is particularly important in deep infections of the plantar surface of the foot, where infection spreads through the tendon sheaths of the toe flexor muscles located in the compartment between the superficial fascia and the arch of the foot.
Debridement should be performed as soon as possible, bearing in mind that in neuroischemic ulcers, formal debridement other than drainage of infection should only be performed after or during revascularization procedures. Be that as it may, recent physiopathological and clinical evidence justifies its use as a useful adjunct to the management of DFIs 65. Whether NPWT actually reduces the bacterial load is debatable, however, its clinical effectiveness in DFIs has been demonstrated. In DFIs, there are no contraindications to NPWT, but special care should be taken to cover exposed blood vessels, prosthesis, or bone with natural tissues or several layers of fine-meshed, non-adherent synthetic material 64.
NPWT should be applied immediately after the revascularization procedure and formal debridement, while the patient is in the operating room. In inpatients, either bed rest or wheelchair use (keeping the affected leg horizontal) is preferred 10,11. Other causes include certain medications, non-compliance, undiagnosed diabetes, substance abuse, and coexisting disease. However, decreased intravascular volume or underlying renal disease decreases the glomerular filtration rate, causing the glucose level to increase.
Patients with DFUs frequently require amputations of the lower limbs and, in more than half the cases, infection is the preponderant factor.
A DFU is any full-thickness wound below the ankle in a diabetic patient, irrespective of duration. 9, however, even with the best of preventive care, 9% of patients with DM will still develop a DFI, with the consequent risk of amputation. It has also been established that perfect and persistent glycemic control, with either insulin or oral agents, stop 13 and probably regress 14 these complications. Once the protective layer of skin is broken, deep tissues are exposed to bacterial colonization. Noninvasive flow studies 17 have demonstrated a hyperperfusion of the foot, especially of the deep tissues, while transcutaneous oxygen pressure (TcPO2) measurements have shown a relative epidermal ischemia as a result of the microvascular dysfunction and arteriovenous shunting 18. This underlines the importance of identifying and aggressively managing associated vascular risk factors, such as obesity, cigarette smoking, dyslipidemia, hypertension, and sedentary behavior 24. Intrinsic traumas are also easily understood as they result from foot deformities (foot drop, equinus, hammertoes, and prominent plantar metatarsal heads) and consequent altered foot biomechanics 4. Consequently, we will only describe the process of wound healing to the degree necessary for the clinician to apply this basic science to selecting treatment interventions and understanding their expected outcomes. Vasoconstriction also promotes a hypoxic and acidotic wound space (secondary to anaerobic metabolism), which stimulates vascular endothelial growth factor (VEGF) release and fibroblast infiltration 38. In diabetic wounds, a persistent inflammatory phase is commonly witnessed at histopathology, which is associated with a delay in the formation of mature granulation tissue and a reduction in wound tensile strength 41. The International Working Group of the Diabetic Foot developed the PEDIS classification system 44, which presents internationally applicable guidelines that can reliably predict the outcome of diabetic foot management 45.
If a possible revascularization is considered, intra-arterial digital subtraction angiography is conducted to properly visualize the arteries of the feet and evaluate the feasibility of revascularization 49. The PEDIS classification system considers the use of a 128-Hz tuning fork applied to the dorsum of the hallux at the base of the proximal phalanx to evaluate the presence or absence of vibration sensation. To definitively categorize the patient into one of these groups different diagnostic procedures are indicated. However, because they are relatively insensitive in the first two weeks, additional imaging studies may be necessary. Plain radiographs should be the initial imaging study, because in established cases, they often show characteristic pathological findings (cortical erosion, periosteal reaction, and mixed lucency and sclerosis). Superficial swabbing of the wound is discouraged, but swabbing the base of the ulcer is acceptable if it is the only possible option 11. Tissue biopsy and fluid aspirate are considered the gold standard for diagnosing wound infection, but deep swabbing of the wound is acceptable in special circumstances.
Even when using these well-defined interfaces, less than 20% of patients are referred to specialized diabetic foot clinics 64. Superficial ulcers without residual ischemia can usually be treated on an outpatient basis. Superficial ulcers without residual ischemia can usually be treated on an outpatient basis with repeated debridement, off-loading, and oral antibiotics. The initial empirical antibiotic therapy in DFIs should aim to cover the most common pathogens and should be based on the known epidemiology of DFIs.
On the other hand, if the infection is not responding then the treatment should be changed to cover all of the isolated organisms. This may be due to either the disruption of microbial synergy or the differential importance of individual virulence potential.
In all other cases, outpatient oral therapy is recommended, provided that regular medical follow-up can be ensured. Published nonrandomized case series on nonsurgical treatment with a prolonged (3 to 6 months) course of antibiotics have reported clinical success in 65% to 80% of cases 10,73. In these later cases, the criterion for revascularization should consider the patient’s status performance, the potential for cicatrization, the site of the lesions, and the quality of the arterial distal runoff. This compartment serves as a non-expandable box, resulting in a compartment syndrome that leads to ischemia and tissue necrosis. Finally, but importantly, a number of studies 65,95,96 suggest that adding NPWT as part of a wound management strategy results in shortened hospital stays and a higher percentage of limb salvage, with consequent decreased overall medical costs.
For the first 2 or 3 days, a continuous suction mode of 125 mmHg should be used and the dressing should be changed every 12 to 24 hours, at which time the wound should be carefully evaluated for any residual necrotic material and subsequent debridement should be performed, if appropriate 64,97. According to a meta-analysis 98, G-CSF treatment might reduce the duration of hospitalization, the risk of lower-limb amputation, and other infection-related invasive intervention, but it does not appear to have a significant effect on the duration of intravenous antibiotic treatment, the resolution of infection, or the rate of wound healing. Physical findings of hyperosmolar hyperglycemic state include those associated with profound dehydration and various neurologic symptoms such as coma. Abdominal distention may occur because of gastroparesis induced by hypertonicity,23 but resolves quickly following adequate rehydration. Given the challenges of treating these complex infections, this paper aims to provide a hospital-based framework for the diagnosis and treatment of diabetic foot infections (DFIs). Based on current studies, the annual population-based incidence is 1 to 4% with a prevalence of 4 to 10%, and the estimated lifetime risk is 25% 2.
This partial failure of prevention strategies supports the need to develop a framework for diagnosing and treating patients with suspected DFIs. DFUs result from a complex interaction of two major risk factors: neuropathy and peripheral vascular disease. Infection is facilitated by DM-related immunological deficits, especially in terms of neutrophils, and rapidly progresses to the deep tissues. The major difference in the diabetic population is the distribution of disease, which tends to be symmetrical with a more distal (tibio-peroneal) involvement and a predominance of long segment occlusions and calcification 25. These foot deformities result from the atrophy induced by motor neuropathy of the foot’s intrinsic muscles.
There are exceptions to this rule of thumb, however, as various organisms have different intrinsic virulence potentials.
In the second stage of the inflammatory phase, leukocytes attracted by chemotaxis, supplant platelets as the dominant cell type.
This new microenvironment, with ECM-embedded fibroblasts coated with a layer of fibronectin, constitutes the scaffolding for the subsequent neo-angiogenesis and re-epithelization. Collagenase and other MMPs degrade Type III collagen, and Type I collagen fibrils are then laid down parallel to the wound lines of tension in an organized fashion, with strong cross-linking and bundle construction, replacing the lost tissue with an increased tensile strength 35.
Continuous bacterial infection 42 and increased advanced glycation end-product (AGE) formation 43 limit the cytokine (mainly TGF-ß)-mediated switch to the later granulation tissue formation phase.
Thus, in clinical practice, the formal revascularization decision is based on information from previous clinical tests and duplex ultrasonography (B mode, color flow and spectral Doppler analysis). Unfortunately, because of the arterial media calcification observed in up to one-third of diabetic patients, this technique has limited usefulness in this special population 47. Magnetic resonance (MR) angiography and computed tomography (CT) angiography, performed without direct arterial injection and without iodinated contrast agent injection for MR angiography, can be alternatives to classic arteriography, especially for distal and calcified lesions. Although both tests have similar sensitivities for evaluating protective sensation loss, and combining modalities appears to increase specificity 51, we consider that, for practical purposes, the 128-Hz tuning fork should be reserved for clarifying equivocal results on the Semmes-Weinstein 10-gram monofilament test in DFI cases.
All patients should have a complete blood count with differential, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) testing and, ideally, procalcitonin (PCT) testing.
Magnetic resonance (MR) imaging, which has a very high sensitivity for bone and deep soft-tissue infections, is preferred to nuclear medicine scans.
However, they are relatively insensitive, particularly in the first two weeks after infection when no changes are frequently found. Independent of the sampling method, specimens must be placed in transport medium and be sent to the microbiology laboratory as quickly as possible. Microbiologists and clinicians working in close collaboration must interpret the results, while taking into consideration the collection conditions, transport time, transport conditions, and the type of bacteria isolated. When a DFI patient presents to the care team, a multidisciplinary management strategy should be rapidly implemented (Figure 7). In other ulcers, formal debridement should be completed and, as accumulating evidence indicates, negative pressure wound therapy (NPWT) should be included in the treatment pathway 65. They should subsequently be refined according to initial response and elements of the patient assessment 29. If the infection is worsening despite susceptibility of the isolated microorganisms, the fastidious organisms may have been missed on culture and a revised debridement should be conducted.
On the other hand, if the infection is not responding then treatment should be changed to cover all the isolated organisms. The optimal duration of antibiotic therapy has not been clearly established, but it could be 1 to 2 weeks for simple forms and 2 to 4 weeks for moderate to severe forms of skin and soft tissue infections. While optimal therapy requires obtaining bone for culture, initial empirical therapy should virtually always cover Staphylococcus aureus, which causes most infections. The current revascularization options for the DM patient include conventional open surgery and endovascular interventions, which are not mutually exclusive and are often combined. Once the infection is controlled and the wound is stable, the suction mode should be changed to an intermittent cycle of 5 minutes on and 2 minutes off.
As there is insufficient evidence to recommend a specific wound dressing or any type of wound healing agent for DFIs, we agree with the National Institute of Health and Clinical Excellence (NICE) guidelines 11 that advise the multidisciplinary team to consider their clinical assessment of the wound, the patient’s preference, clinical circumstances, and acquisition cost. Systemic HBOT has also been proposed, as infection and ischemia are considered the two main indications for this procedure.
The first step of treatment involves careful monitoring of the patient and laboratory values. Abdominal distention that persists after rehydration may be related to other underlying causes.Various changes in mental status may manifest, ranging from complete lucidity to disorientation to lethargy to coma. According to a study published by the Eurodiale study group 3, approximately 58% of DFU patients will become clinically infected.

This assumes special importance in DFIs that require hospitalization, as strategies have proven efficacy in reducing morbidity, mortality, psychological distress, and financial costs10. Neuropathy, both symmetric and bilateral, plays the main role with varying degrees of alterations in autonomic, sensory, and motor functions. When femoral disease is present, it tends to be diffuse with no single dominant focal lesion 23.
Anaerobes are rarely the sole pathogen, but they often participate in a mixed infection with aerobes, especially in cases of deep tissue infection 30.
A good example is ß-hemolytic streptococci which is able to induce tissue damage at 102 CFU per gram of tissue, while greater counts of less pathogenic organisms may be of little clinical significance 32.
Neutrophils are the first to begin bactericidal activities, using inflammatory mediators and oxygen free-radical metabolites. Initially directed by fibroblasts that express keratinocyte growth factor-2 (KGF-2) and interleukin-6 (IL-6), and later by nitric oxide (NO) and IL-6 self-expression, keratinocytes at the wound edges migrate laterally along the basal membrane and both proliferate and differentiate to produce the epidermis 36. This results in prolonged inflammation and increased neutrophil infiltration with consequent protease activity. The complexity and cost of toe pressure or TcpO2 use precludes their generalized application outside clinical studies. On the other hand, more complex techniques, such as systolic toe-pressure measurement or TcPO2, were better predictors of healing in several studies 25. The cause and severity gradation of protective sensory loss are difficult to evaluate and do not provide clinically useful information 15, consequently, they are not considered necessary.
However, caution must be exercised when interpreting laboratory tests, as no marker is sufficiently sensitive and specific to confirm the diagnosis of DFI and tests are often misleading, even in the case of severe lesions 19. The gold standard for diagnosing osteomyelitis remains histopathology of a positive culture from a properly obtained bone specimen. Furthermore, they are nonspecific, because they do not permit the differential diagnosis of noninfectious neuro-osteoarthropathy 58. Despite its high cost, this imaging test has gained wide acceptance in the management of patients with DFI 60, as it can also be used for surgical planning.
Assuming that there are no completely reliable microbiological methods to distinguish between pathogenic and nonpathogenic microorganisms at the present time, microbiologists and clinicians must collaborate closely to interpret the results.
As previously described, evidence suggests that this reduces the incidence of major amputation. Accumulating evidence also suggests that negative pressure wound therapy (NPWT) should be included in the treatment pathway.
The severity of infection is essential in determining the appropriate antibiotic regimen 10. If the infection is worsening despite the isolated microorganisms’ susceptibility, the possibility that fastidious organisms were missed on culture should be taken in account and a revision of debridement should be done. Cost is also an important consideration, and antibiotic therapy should proceed as indicated by the clinical situation and severity of the infection, with the lowest cost. The traditional recommendations of initial parenteral therapy may be outdated by the introduction of newer agents with excellent oral bioavailability 29. Open surgical techniques include endarterectomy for local lesions and peripheral bypass for long occlusions. 87 showed that NPWT use resulted in enhanced granulation tissue formation with improved bacterial clearance compared with control dressings.
The dressings should then be changed every 24 to 48 hours, as this has been shown to increase blood flow and improve granulation 86. Its use was recently analyzed in a systematic review 99 of five RCTs in which it was associated with a reduction in major amputations, but not in minor amputations or time to heal. Vigorous correction of dehydration with the use of normal saline is critical, requiring an average of 9 L in 48 hours.
The degree of neurologic impairment is related directly to the effective serum osmolarity,15 with coma often occurring once the serum osmolarity is greater than 350 mOsm per kg (350 mmol per kg).
We stress the need for a clinical diagnosis of DFIs and the importance of microbiological evaluation for antibiotic therapy guidance.
Patients with DM frequently require minor or major amputations of the lower limbs (15 to 27%) and in more than 50% of cases, infection is the preponderant factor 4.
Despite the publication of different clinical guidelines for DFI management, there is still practical variation in inpatient management 10,11. Playing a secondary role is peripheral vascular disease resulting from atherosclerosis (Figure 1). Contrary to the classical conceptualization, it is of the utmost importance to recognize that most diabetic persons have adequate circulation necessary for a cure 17. These mixed infections provide an optimal opportunity for microbial synergy, which increases the net pathogenic effect and hence the severity of infection 28.
A third critical factor is the efficacy of the host’s immune response in dealing with wound microflora. As these begin to wane, circulating monocytes, attracted by TGF-ß and PDGF, enter the wound and mature into tissue macrophages. In turn, keratinocytes direct neo-angiogenesis at the wound edge by expressing VEGF, which is upregulated by NO. In these patients, the most sensible sign of infection is often recalcitrant hyperglycemia despite regular anti-hyperglycemic regimens. Newer techniques, such as positron emission tomography (PET) scans, appear promising, but their role is as yet undefined 61. They must also take into account the collection conditions transport time, transport conditions, and the type of bacteria isolated. Assuming that debridement, infection, ischemia, offloading, and nutritional status are addressed, a wound that fails to improve within 2 to 4 weeks should prompt the clinician to consider alternative and adjunctive therapies. Patients with mild infections who have not previously received antibiotic therapy usually have an infection caused by only one or two species of bacteria 68, and an antibiotic regimen should almost always include an agent active against Staphylococcus aureus and Streptococcus spp. Understanding these basic principles behind choosing an antibiotic regimen is more important than knowing particular antibiotic regimens, and each hospital should have epidemiology-based antibiotic guidelines for DFI management.
For bypass surgery, a single segment of the greater saphenous vein is the best conduit, although acceptable results have been obtained with prosthetic grafts that do not cross the knee 74. The debridement process involves physically excising necrotic material and debris until normal tissue appears, thus enabling wound healing and removing a reservoir of potential pathogens 79. In other studies 88, NPWT reduced the bacterial count to 104 to 106 per gram of tissue within 4 to 5 days. Regarding treatment, we propose a multidisciplinary approach prioritizing invasive infection drainage, necrosis debridement, and the prompt start of empirical antibiotic therapy, followed by complete and appropriate vascular reconstruction. Major amputation is associated with significant morbidity and mortality (ranging from 13 to 40% at 1 year to 39 to 80% at 5 years 2) in addition to immense social, psychological, and financial consequences 5.
This paper aims to provide a hospital-based framework for the diagnosis and treatment of DFIs, based on a pathophysiological approach. In this time frame, in which autonomic dysfunction dominates, there is clinically a pathophysiologically resultant hot and turgid foot.
Accordingly, the composition of the polymicrobial wound flora is likely to be more important than the presence of specific pathogens. In DFUs, infection is facilitated by intrinsic immunological deficits, especially in terms of neutrophil dysfunction. These cells debride the wound on a microscopic level and produce cytokines necessary for the proliferative stage 36. The vasodilation induced by NO also aids in the movement of inflammatory cells to the site of injury. In our clinical experience, CRP has proven to be a good test in the diagnosis and follow up of serious DFIs.
The criterion gold standard for diagnosing osteomyelitis is a characteristic histopathology (acute or chronic inflammatory cells, or necrosis) associated with a positive culture from a properly obtained bone specimen ideally obtained at the time of surgical debridement or by fluoroscopic- or computed tomography-guided percutaneous biopsy 55. These professionals should also have access to other specialist services such as those provided by vascular surgeons and orthopedists 11. A biomechanically sound reconstruction, with or without amputation, should be part of the treatment plan to minimize the risk of recurrent ulceration. Long-term results are good, with 5-year secondary patency rates >70% and limb salvage rates of 75 to 85% 75. 10 that only additional randomized clinical trials can establish protocols for using these expensive and limited resources to treat DFIs. For severe DFIs, we suggest that negative pressure wound therapy (NPWT) be included in the treatment pathway. Signs or symptoms of vascular compromise are observed in 40 to 50% of all patients with the vast majority having neuroischemic ulcers, and only a minority of patients have purely ischemic ulcers 15. In comparison, culture results from associated soft tissue wounds or sinus tracts do not reliably correlate with those taken from bone 60. Long-standing or severe DFIs need extended coverage to include commonly isolated Gram-negative bacilli, Enterococcus spp., and anaerobes. Although it’s not currently advisable for most clinically infected chronic wounds, it may have a role in specific circumstances 70. 89 showed that despite the clear beneficial effects of NPWT, bacterial colonization increased significantly within the range of 104 to 106 per gram of tissue during prolonged therapy.
If these treatments fail or are not considered, amputation remains the only option in cases of severe infection, especially in the neuroischemic foot. Sensory neuropathy begins with poorly tolerated tactile allodynia and thermal hyperalgesia.
Recognizing the insensibility of classical signs and laboratory tests for the diagnosis of DFI and that various factors suggest the presence of DFI in the absence of these classical signs 53, Lipsky et al.
The application of any topical antibiotic should always be preceded by formal debridement and may be considered for a properly managed wound with subclinical infection that is failing to heal or to help in the removal of biofilms, which have been implicated in persistent infections 71.
This treatment modality has a number of advantages over bypass surgery, particularly its low morbidity and mortality rate.
It is our hope that this protocol will improve the hospital management of DFIs and, ultimately, the prognosis of DFI patients.
As progressively thicker myelinated fibers are affected this progresses to an objective loss of sensation and proprioceptive dysfunction 20.
However, the restenosis rate is relatively high, especially in below-the-knee procedures for which it is as high as 50% over a 5-year period 76. They should implement the technique that best matches their specialist expertise and clinical experience, the patient’s preference, and the site of the ulcer 11.
90, in which NPWT was compared with conventional moist dressing therapy and did not significantly decrease the total bacterial load. Finally, physicians should focus on preventing future episodes using patient education and instruction in self-monitoring. Motor neuropathy results from the axonal degeneration of the large motor myelinated fibers. Since the main goal for patients with DFI is to obtain sufficient perfusion to control the infection and save the limb, this is significant since this temporary improvement of perfusion can be sufficient enough to promote healing and avoid amputation. Efforts should be made to only remove dead tissue, while preserving as much other viable tissue as possible.
There were qualitative differences, however, with nonfermentative Gram-negative bacilli showing a significant reduction and Staphylococcus aureus showing a significant increase.
This causes anterior crural muscle atrophy or intrinsic muscle wasting, which leads to foot deformities and consequent altered foot biomechanics with foot pressure redistribution 19. However, it takes up to 28 days after endovascular intervention for the new blood flow to have maximal effect at the wound’s edge, whereas this time frame is reduced to 4 to 10 days after bypass surgery 77.
Sharp debridement with a scalpel, scissors, or tissue nippers is the conventional procedure; however, to minimize damage to normal tissue, which sometimes occurs with normal surgical sharp debridement techniques, alternative debridement with a hydrosurgical water knife may be used 81. This suggests that bacterial burden reduction may occur within the first 4 to 5 days, making subsequent therapy effective in decreasing wound size. Details about the addition of potassium to the intravenous fluids are provided in the next section.Once there is only mild hypotension, the corrected serum sodium level should be calculated.
As the disease progresses, the foot becomes clinically insensitive and possibly deformed (claw toes, hammertoes, prominent metatarsal heads, etc.). The results of recent studies 78 indicate that endovascular therapy might take a prominent place in the treatment of PAD, especially in patients with significant comorbidities, and this applies even more to patients with DFI. In all of the procedures, serial thin slices of tissue should be removed until normal tissue appears. This was also seen in the first large prospective and randomized study of NPWT use in the treatment of complex clean diabetic foot wounds 83. Antiplatelet therapy should begin preoperatively and continue after an endovascular or surgical procedure 25. If the corrected serum sodium level is low (less than 135 mEq per L), 0.9 percent sodium chloride is infused at the same rate. Good clinical judgment should be employed, especially when the patient has comorbid conditions such as acute myocardial infarction, a history of congestive heart failure, or renal failure. For this reason, the rate at which serum tonicity is returned to normal should be somewhat slower than in adults.28ELECTROLYTE MANAGEMENTElectrolyte replacement is critical.
Total body potassium depletion often is unrecognized10 because the level of potassium in the blood may be normal or high.13 The serum potassium level may plummet when insulin is replaced because this forces potassium into the cell.
Most studies1,5,10 that have examined the need for phosphate replacement involved patients with diabetic ketoacidosis that developed over hours to days. Because phosphate replacement can cause severe hypocalcemia in this setting, serum calcium levels should be monitored closely.25Hypomagnesemia may manifest as arrhythmias, muscle weakness, convulsions, stupor, and agitation. If insulin is administered before fluids, the water will move intracellularly, causing potential worsening of hypotension, vascular collapse, or death.
If the glucose level does not decrease by 50 to 70 mg per dL per hour, this rate of administration may be doubled.
Once the serum glucose concentration is below 300 mg per dL, dextrose should be added to the intravenous fluid and insulin should be titrated by a low-dose sliding scale until the mental obtundation and hyperosmolarity are resolved. When the patient is able to eat, subcutaneous insulin or the previous treatment regimen may be initiated.1IDENTIFY AND TREAT THE CAUSEAlthough routine administration of antibiotics for all patients with suspected infection is not recommended, antibiotic therapy is warranted while awaiting culture results in older patients or in those with hypotension.
According to a recent study,29 elevated C-reactive protein and interleukin-6 levels are early indicators of sepsis in patients with hyperosmolar hyperglycemic state.It also is important to review any medications that may have precipitated or aggravated the event, and discontinue or reduce the dosage of any suspected agent.

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  2. AnTiS

    Monitor their blood glucose levels.Type 1 diabetes is much happens when a diabetic is already once you're in ketosis.