Hyperglycemic crisis and diabetic foot ulcers -
Some patterns, such as unequal revascularization rates in people with ischemic DFU, have been shown to widen among the highest-income Black and White adults These findings reflect gaps in our ability to measure racial biases within the health system. Geographic variation in lower-extremity outcomes is well established and is closely linked to socioeconomic status.
In the U. and U. Differential access to preventive and specialty care 59 , 61 , financial constraints that delay presentation 62 , and provider-specific practices in limb preservation 54 likely contribute to geographic disparities and to worse outcomes in minority and rural populations 49 , Some health system-based measures, including managed care plans and Medicaid expansion, have demonstrated modest narrowing of disparities in DFU morbidity 26 , 63 , although dedicated research on interventions to specifically address disparities is lacking.
The cumulative burden of hyperglycemia and its causal relationship with microvascular complications are well established Chronically elevated HbA 1c is an independent risk factor for DFU and for amputation and mortality following DFU Maintaining a lower HbA 1c delays the progression of microvascular complications of diabetes 65 , 66 and is associated with decreased risk of amputation in adults with type 1 and type 2 diabetes Secondary analyses and extended follow-up of landmark trials show dose-response associations between HbA 1c and risk of incident DFU and amputation The association of obesity with incident DFU has not been consistently demonstrated, and obesity is not associated with incident or recurrent DFU, amputation, or mortality in several recent systematic reviews 30 , 38 , 41 , In patients who develop DFU, underweight BMI has been linked to an increased risk of amputation and mortality in population- and hospital-based studies 17 , 41 , likely reflecting higher rates of frailty and poor nutrition in the underweight population.
Smoking is associated with an increased risk of PN in adults with diabetes and is an extremely strong risk factor for PAD Several studies report strong associations of smoking with incident DFU 30 , longer healing time, higher rates of nonhealing DFU 18 , and a subsequent 1.
Prospective cohorts demonstrate bidirectional associations between DFU and cardiovascular disease, with incident DFU associated with faster progression of cardiovascular disease 69 , and even subclinical cardiovascular disease conferring increased risk of DFU Cardiovascular disease is also associated with delayed healing and a higher risk of amputation and mortality 4 , DFU and cardiovascular disease are both markers of diabetes severity and duration, and they act synergistically on physiologic e.
Aggressive management of cardiovascular risk factors is a central goal of multidisciplinary diabetes care and has been shown to decrease risk of DFU occurrence and reduce mortality in people who develop DFU Diabetes is a leading global cause of chronic kidney disease CKD and the most common cause of end-stage kidney disease Black and Hispanic adults and low-income groups have much higher rates of CKD than White and middle- or high-income groups End-stage kidney disease and CKD are linked to higher risk of incident DFU, longer healing time, higher ulcer recurrence rates, and higher rates of lower-extremity amputation 76 , These associations are strong enough to warrant inclusion of CKD in expert definitions of an at-risk foot even for people without prior DFU or structural deformity.
For people with kidney disease, end-stage kidney disease on hemodialysis confers the greatest risk of DFU The high prevalence of CKD among racial and ethnic minorities and socioeconomically disadvantaged people contributes to the disproportionate burden of DFU morbidity in these populations.
There is a strong association between the presence and severity of diabetic retinopathy and DFU. Diabetic retinopathy occurs at two- to fourfold higher rates among adults with DFU than in those without Visual impairment secondary to retinopathy may worsen gait instability and increase risk of foot trauma in those with PN, which can precipitate DFU formation 78 , although the causal mechanisms have not been definitively established.
Both DFU and retinopathy are likely signs of advanced microvascular disease that may partially explain this association. Ulcer healing is defined as complete epithelialization of a previously ulcerated site Time from diagnosis to wound healing and overall rates of healing differ widely based on ulcer etiology, size, presence of infection, and patient characteristics, with median healing times ranging from 3 months to more than 12 months 7 , Ischemic ulcers, larger and deeper ulcers, plantar ulcers, and ulcers with infection are associated with poor or prolonged healing 7 , 18 , 81 , In addition to wound- and patient-level risk factors described previously, nonambulatory status is associated with prolonged healing and lower amputation-free survival 7 , There is currently no validated predictive model for DFU healing that includes both patient and wound factors.
The strongest clinical predictor of developing a DFU is a prior DFU or amputation 2. Recurrence is the occurrence of an ulcer, either at the site of a prior ulcer or at another site, after complete healing 5. Contralateral lower-extremity amputation independently increases ulcer recurrence by two- to threefold and shortens the average interval to ulcer recurrence 84 , presumably due to gait alterations.
Other factors consistently associated with recurrence are similar to those for nonhealing, although PAD has not been shown to be a strong influence on DFU recurrence despite its effects on primary healing Infection is a primary driver of emergency department visits and hospitalization in patients with diabetes and with DFU specifically 86 , Foot ulcer precedes the vast majority of diabetic foot infections, with higher risk of infection in recurrent wounds, long-standing wounds, and wounds that probe to bone, as well as among patients with recent history of prior non—foot infection 70 , 85 , Diabetes is the leading risk factor for lower-extremity amputation in U.
adults, with an estimated , diabetes-related major or minor amputations per year Overall diabetes-related amputations decreased steadily over the s and s despite rising diabetes prevalence.
Over the same time, minor amputation made up an increasing proportion of these amputations, corresponding to higher rates of lower-extremity revascularization procedures; these trends are thought to represent improved efforts at limb preservation 91 , The overall resurgence in severe morbidity appears to disproportionately affect younger adults and Black and Hispanic groups 42 , 53 , 55 , 94 , which is particularly concerning given the already wide inequities in care for racial and ethnic minorities.
Even controlling for DFU incidence, Black and Hispanic adults have lower rates of attempted revascularization, higher rates of failed limb preservation, and higher risk of amputation than White adults 49 , 50 , 52 , Amputation is a late-stage complication of poor long-term diabetes management, and it often reflects inadequate access to, delivery of, and uptake of diabetes care.
The compounding effects of socioeconomic disadvantage, other social determinants of health, and structural racism on marked disparities in amputation rates by race, ethnicity, and socioeconomic status cannot be overstated 35 , Survival in people with incident DFU is significantly worse compared with that of similar people with diabetes without foot complications 2 , A recent meta-analysis comprising almost , patients in 16 countries reported mortality rates of Diabetes care in the U.
These numbers likely underestimate the true economic burden of DFU given out-of-pocket expenses, loss of productivity, and decreased employment associated with DFU Prevention and management of diabetic foot complications is a centerpiece of diabetes care.
A discussion of best-practice diabetes care is beyond the scope of this review, but many DFU-associated metabolic and cardiovascular risk factors are modifiable in early stages and are addressed by clinical guidelines and Europe Delayed ulcer presentation predicts poor prognosis 7 , 54 , Frequent foot exams are fundamental to decreasing incidence and morbidity, and inadequate foot care is associated with higher rates of DFU, LEA, and mortality , Guidelines for frequency of screening for PN, PAD, and DFU or other preulcerative lesions in the adults with diabetes Table 2 recommend at least an annual comprehensive foot exam for all patients with diabetes, including inspection, monofilament and tuning fork evaluation for loss of protective sensation, and pulse exam 1 , Screening exams should be performed every 3—6 months for high-risk patients The importance of multidisciplinary foot care for high-risk people deserves particular emphasis, especially the involvement of podiatry and vascular surgery Rates of annual foot exams by a provider in adults with diabetes vary widely Certain racial and ethnic minority populations e.
The implementation of a hemodialysis center-based monthly foot screening in a U. Routine foot screening is critical and low rates of adherence to standards of care for preventing diabetic foot infections is a major concern.
Several promising technologies may aid in the early detection of preulcerative or ulcerative foot lesions. Telemedicine-assisted foot examinations have been shown in small studies to be as effective as in-person provider exams at detecting early lesions, with time and cost savings to patients that have promise to reduce existing barriers to care 62 , Increased temperature is a well-validated preulcerative sign, and clinical trials of temperature-sensing mats and socks have been successful in identifying preulcer or DFU weeks earlier than a clinical exam.
These passive surveillance technologies may be able to reduce incident DFU through alerts to offload pressure points temporarily or by prompting a thorough foot evaluation.
Additional pressure-sensing modalities including insoles may help risk-stratify people with high plantar pressures, monitor for effective offloading before or during DFU episodes, and evaluate progress in gait retraining after DFU healing or amputation Despite compelling evidence supporting their efficacy and cost effectiveness, these technologies have not been widely adopted.
The detrimental effect of DFU on overall health status and quality of life is well documented, and patient-reported outcomes are increasingly recognized as meaningful measures in diabetic foot care , People with DFU typically report poor quality of life, primarily in the domain of physical functioning.
Persistent ulcers, major amputation, and limited ambulation are associated with worse quality of life for both patients and their caregivers , Healing, including after minor amputation, is associated with dramatic improvement in self-reported physical functioning, and people with healed DFU have overall self-reported quality of life near the norms for populations without diabetes Though qualitative studies consistently identify fear, anxiety, frustration, isolation, and sadness as common emotional responses to the diagnosis of DFU, few studies have demonstrated differences in psychosocial quality of life related to DFU DFU-specific measures have been proposed to better assess the social and emotional consequences of active ulcers and should be considered when evaluating patient-reported outcomes.
DFU is a common complication of diabetes that has been aptly compared with cancer in terms of chronicity, recidivism, cost, and burden Major clinical risk factors for DFU are PN, PAD, and foot deformities, but race, ethnicity, socioeconomic status, and geography are powerful mediators of risk for DFU and lower-extremity amputation.
The consequences of first ulceration—poor quality of life, recurrence, major amputation, and death—are significant, but this morbidity is not reflected in the funding allocated for DFU-related research, which totals less than 0.
Complications of DFU can be attenuated by guideline-directed screening, early diagnosis, and aggressive medical management of diabetes and cardiovascular disease. Ineffective population-based screening, limited access to preventive care, and delays in access to diabetes, vascular, and podiatry specialist care contribute to late-stage ulcer presentation and, thus, to poor prognosis.
Rising lower-extremity amputation rates among young and middle-aged adults with diabetes and persistent racial, ethnic, and socioeconomic disparities reflect these gaps in care. Major efforts are needed to develop health system-wide improvements in DFU prevention and early diagnosis, especially in disadvantaged populations.
Funding should be prioritized for high-quality population-based registries to track DFU incidence, prevalence, outcomes, and process measures. Initiatives to expand use of effective at-home screening modalities and allocate resources for more frequent provider foot exams in regions where major amputation rates are high have the potential to reduce DFU incidence and morbidity in the most at-risk populations.
Dedicated research on racial and socioeconomic differences in timing of care, limb preservation, and amputation are necessary to identify and address factors perpetuating structural bias and disparate outcomes.
Significantly more public and institutional funding for DFU research and care initiatives is warranted to correct the imbalance between current resource allocation and the enormous burden of DFU.
Ultimately, a paradigm shift toward DFU prevention and health equity is required to produce meaningful reductions in DFU, major lower-extremity amputation, and mortality. We acknowledge the contributions of Caroline Wang Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD and Alana Keegan Division of Vascular Surgery and Endovascular Therapy, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD in creating and editing figures and tables.
was supported by National Institutes of Health NIH National Institute of Diabetes and Digestive and Kidney Diseases NIDDK grant K23 DK was supported by NIH National Heart, Lung, and Blood Institute grant K24 HL This work was also supported by NIH NIDDK grant R01 DK to L. Duality of Interest. No potential conflicts of interest relevant to this article were reported.
Author Contributions. completed literature review and wrote the manuscript. and A. reviewed and edited the manuscript. and C. were involved in the conception of this work and reviewed and edited the manuscript. All authors approved of the final version of the manuscript.
are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
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Volume 46, Issue 1. Previous Article Next Article. Presentation, Etiology, and Characterization of Diabetic Foot Ulcers. Wound Classification and Staging. Epidemiology of Diabetic Foot Ulcers. Risk Factors for DFU and Associated Morbidity. Morbidity and Mortality Related to DFU.
Economic Burden of DFU. Primary and Secondary Prevention of DFU. Quality of Life and Functional Impact of DFU. Article Information. Article Navigation. Review December 22 Etiology, Epidemiology, and Disparities in the Burden of Diabetic Foot Ulcers Katherine McDermott X.
Katherine McDermott. This Site. Google Scholar. Michael Fang ; Michael Fang. Andrew J. Boulton ; Andrew J. Elizabeth Selvin Elizabeth Selvin. Caitlin W. Hicks Corresponding author: Caitlin W. Hicks, chicks11 jhmi. Diabetes Care ;46 1 — Article history Received:. Get Permissions.
toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Graphical Abstract View large Download slide. View large Download slide. Figure 1. Figure 2. Person- and foot-specific factors interact to promote DFU risk and poor clinical outcomes.
Figure 3. Table 1 Description and summary of benefits and limitations for common existing diabetic foot and limb classification systems. Assigns a clinical stage that estimates risk of amputation from 1 very low to 4 very high based on the combination of these factors stage 5: unsalvageable limb.
Extensively validated in diverse settings where data may be limited Unique in its inclusion of ulcer location High scores predictive of healing and LEA Has broad applications for use in population-based studies or resource-poor settings Dichotomized variables limit assessment of change over time or of the relative contribution of severe features e.
Assigns 1 present or 0 absent for location, ischemia, peripheral neuropathy, infection, area, and depth. Extensively validated in diverse settings Unique in its inclusion of ulcer location High scores predictive of healing and LEA Has broad applications for use in population-based studies or resource-poor settings where data may be limited Dichotomized variables limit assessment of change over time or of the relative contribution of severe features e.
View Large. Figure 4. Pathways to ulceration and lower-extremity amputation in DFU. Table 2 Professional guidelines for screening and management of patients at risk for DFU.
Foot exams. International Diabetes Federation. Brussels, Belgium, International Diabetes Federation, Accessed 1 August Search ADS. Prevalence, clinical aspects and outcomes in a large cohort of persons with diabetic foot disease: comparison between neuropathic and ischemic ulcers.
van Netten. Comparison of characteristics and healing course of diabetic foot ulcers by etiological classification: neuropathic, ischemic, and neuro-ischemic type. Diabetic foot ulcers and vascular insufficiency: our population has changed, but our methods have not.
Decreasing incidence of foot ulcer among patients with type 1 and type 2 diabetes in the period Diabetic neuropathy: a position statement by the American Diabetes Association. Epidemiology of peripheral neuropathy and lower extremity disease in diabetes. Global vascular guidelines on the management of chronic limb-threatening ischemia.
Epidemiology and risk of amputation in patients with diabetes mellitus and peripheral artery disease. Peripheral arterial disease in diabetic and nondiabetic patients: a comparison of severity and outcome.
The management of diabetic foot: a clinical practice guideline by the Society for Vascular Surgery in collaboration with the American Podiatric Medical Association and the Society for Vascular Medicine.
Foot ulcer and risk of lower limb amputation or death in people with diabetes: a national population-based retrospective cohort study.
Diabetic Foot Working Group, Queensland Statewide Diabetes Clinical Network, Australia. Factors associated with healing of diabetes-related foot ulcers: observations from a large prospective real-world cohort. Prediction of outcome in individuals with diabetic foot ulcers: focus on the differences between individuals with and without peripheral arterial disease.
The EURODIALE Study. The Society for Vascular Surgery lower extremity threatened limb classification system: risk stratification based on wound, ischemia, and foot infection WIfI.
Diabetic foot ulcer incidence and survival with improved diabetic foot services: an year study. Preventing foot ulceration in diabetes: systematic review and meta-analyses of RCT data. Development and validation of an incidence risk prediction model for early foot ulcer in diabetes based on a high evidence systematic review and meta-analysis.
Rates of diabetes-related major amputations among racial and ethnic minority adults following Medicaid expansion under the Patient Protection and Affordable Care Act.
Incidence, hospitalization and mortality and their changes over time in people with a first ever diabetic foot ulcer. Incidence of diabetic foot ulcer in Japanese patients with type 2 diabetes mellitus: the Fukuoka diabetes registry.
Epidemiology of foot ulceration and amputation: can global variation be explained? Global epidemiology of diabetic foot ulceration: a systematic review and meta-analysis.
Global recurrence rates in diabetic foot ulcers: a systematic review and meta-analysis. Trends in receipt of American Diabetes Association guideline-recommended care among U. adults with diabetes: NHANES Socioeconomic inequalities and type 2 diabetes complications: a systematic review.
An illustration of some commonly described abnormalities is shown in Figure 1. In examining for vascular abnormalities of the foot, the dorsalis pedis and posterior tibial pulses should be palpated and characterized as present or absent.
If vascular disease is a concern, measuring the ankle brachial index ABI can be used in the outpatient setting for determining the extent of vascular disease and need for referral to a vascular specialist.
The ABI is obtained by measuring the systolic blood pressures in the ankles dorsalis pedis and posterior tibial arteries and arms brachial artery using a handheld Doppler and then calculating a ratio.
Ratios below 0. However, in patients with calcified, poorly compressible vessels or aortoiliac stenosis, the results of the ABI can be complicated. The loss of pressure sensation in the foot has been identified as a significant predictive factor for the likelihood of ulceration.
A screening tool in the examination of the diabetic foot is the gauge monofilament. The monofilament is tested on various sites along the plantar aspect of the toes, the ball of the foot, and between the great and second toe.
The test is considered reflective of an ulcer risk if the patient is unable to sense the monofilament when it is pressed against the foot with enough pressure to bend it.
The results of the foot evaluation should aid in developing an appropriate management plan. These classification systems are based on a variety of physical findings. One of the most popular systems of classification is the Wagner Ulcer Classification System, which is based on wound depth and the extent of tissue necrosis Table 1.
The University of Texas system is another classification system that addresses ulcer depth and includes the presence of infection and ischemia Table 2. The management of diabetic foot ulcers includes several facets of care. Offloading and debridement are considered vital to the healing process for diabetic foot wounds.
There are multiple methods of pressure relief, including total contact casting, half shoes, removable cast walkers, wheelchairs, and crutches. There are advantages and disadvantages to each modality, and factors such as overall wound condition, required frequency for assessment, presence of infection, and the likelihood for patient compliance should be considered in determining which modality would be most beneficial to the patient.
The open diabetic foot ulcer may require debridement if necrotic or unhealthy tissue is present. The debridement of the wound will include the removal of surrounding callus and will aid in decreasing pressure points at callused sites on the foot.
Additionally, the removal of unhealthy tissue can aid in removing colonizing bacteria in the wound. It will also facilitate the collection of appropriate specimens for culture and permit examination for the involvement of deep tissues in the ulceration.
The selection of wound dressings is also an important component of diabetic wound care management. There are a number of available dressing types to consider in the course of wound care. Although there is a dearth of published trials to support the use of one type of dressing compared to another, 26 the characteristics of specific dressing types can prove beneficial depending on the characteristics of the individual wound.
Saline-soaked gauze dressings, for example, are inexpensive, well tolerated, and contribute to an atraumatic, moist wound environment. Foam and alginate dressings are highly absorbent and can aid in decreasing the risk for maceration in wounds with heavy exudates.
A complete discussion of the various classes of wound dressings is beyond the scope of this review; however, an ideal dressing should contribute to a moist wound environment, absorb excessive exudates, and not increase the risk for infections.
If infection is suspected in the wound, the selection of appropriate treatments should be based on the results of a wound culture. Tissue curettage from the base of the ulcer after debridement will reveal more accurate results than a superficial wound swab.
Gram-positive cocci are typically the most common pathogens isolated. However, chronic or previously treated wounds often show polymicrobial growth, including gram-negative rods or anaerobes. Pseudomonas, for example, is often cultured from wounds that have been soaked or treated with wet dressings.
Anaerobic bacteria are often cultured from ulcers with ischemic necrosis or deep tissue involvement. Antibiotic-resistant organisms such as methicillin-resistant staphylococcus aureus are frequently found in patients previously treated with antibiotic therapy or patients with a recent history of hospitalization or residence in a long-term care facility.
The selection of appropriate antimicrobial therapy, including the agent, route of administration, and need for inpatient or outpatient treatment will be determined in part by the severity of the infection. Clinical signs of purulent drainage, inflammatory signs of increased warmth, erythema, pain and induration, or systemic signs such as fever or leukocytosis should be considered.
Patients with systemic signs of severe infection should be admitted for supportive care and intravenous antibiotic therapy; additionally, a surgical evaluation is warranted to evaluate for a deep occult infection.
In the absence of serious signs, patients can be treated with outpatient therapy and frequent follow-up. Information about specific agents that have shown clinical effectiveness and suggested treatment schemes based on infection severity has been published elsewhere.
The possibility of underlying osteomyelitis should be considered with the presence of exposed bone or bone that can be palpated with a blunt probe.
If osteomyelitis is diagnosed, the patient may undergo surgical excision of the affected bone or an extensive course of antibiotic therapy. Consideration is also given to the presence of underlying ischemia because an adequate arterial blood supply is necessary to facilitate wound healing and to resolve underlying infections.
Patients with evidence of decreased distal blood flow or ulceration that does not progress toward healing with appropriate therapy should be referred to a vascular specialist. Upon determination of the patient's anatomy and a vascular route amenable to restoration, the patient may undergo arterial revascularization.
Surgical bypass is a common method of treatment for ischemic limbs, and favorable long-term results have been reported. A number of adjunctive wound care treatments are under investigation and in practice for treating diabetic foot ulcers.
The use of human skin equivalents has been shown to promote wound healing in diabetic ulcers via the action of cytokines and dermal matrix components that stimulate tissue growth and wound closure. Two of the more popular adjunctive therapies in use are hyperbaric oxygen therapy HBOT and the use of granulocyte colony stimulating factors G-CSF.
HBOT is the delivery of oxygen to patients at higher than normal atmospheric pressures. This results in an increase in the concentration of oxygen in the blood and an increase in the diffusion capacity to the tissues.
The partial pressure of oxygen in the tissues is increased, which stimulates neovascularization and fibroblast replication and increases phagocytosis and leukocyte-mediated killing of bacterial pathogens in the wound.
Presently, there are conflicting data regarding the efficacy of this therapy. Although small randomized studies have demonstrated an improvement in the rate of wound healing and a decrease in the number of amputations, 37 , 38 other studies contest these data.
The quality of the studies to date has been poor, and their findings have not been confirmed in a large, blinded, and adequately powered randomized trial.
Diabetic wounds that meet the appropriate criteria are classified as Wagner Grade 3 wounds that have failed to resolve after a day course of standard treatment. The use of G-CSF is another new adjunctive therapy under investigation. G-CSF has been found to enhance the activity of neutrophils in diabetic patients.
A meta-analysis of these studies 41 revealed that, although the use of G-CSF did not significantly accelerate the resolution of infection in diabetic wounds, there was a decreased likelihood of amputation and the need for other surgical therapies in treated wounds.
Early detection of potential risk factors for ulceration can decrease the frequency of wound development. It is recommended that all patients with diabetes undergo foot examinations at least annually to determine predisposing conditions to ulceration.
A risk classification scheme has been created in the report of the task force of the Foot Care Interest Group of the ADA 13 that is reportedly designed to make basic recommendations regarding the need for specialist referral and the frequency of follow-up by primary providers and specialists Table 3.
Patients in the lowest risk category are recommended to receive education on general foot care and annual follow-up. Increasing risk categories require more components of care and are more likely to benefit from specialist care and follow-up.
A recommended frequency of follow-up for each risk category is also included in the table; follow-up increases in frequency with an increase in risk category. Patients with diabetes are at an increased risk for developing foot ulcerations. The consequences of persistent and poorly controlled hyperglycemia lead to neuropathic and vascular abnormalities that cause foot deformities and ulceration.
The feet of diabetic patients should be examined at least annually to determine predisposing conditions to ulceration. Treatment plans should be based on examination findings and the individual risk for ulceration.
If ulcers are present, the treatment strategy should include offloading, debridement, and appropriate dressings. Further, the presence of infections should be determined by clinical findings and appropriate wound cultures and treated based on the culture results.
If evidence for ischemia is present, revascularization may be indicated to restore arterial blood flow and increase the chance for limb salvage.
There are adjunctive therapies available that can also contribute to the overall healing process of the wounds in affected patients. By conducting a periodic foot survey in diabetic patients and incorporating the appropriate basic and specialized care as warranted, the risk of ulceration and its associated morbidities can be reduced.
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Volume 27, Issue 2. Previous Article Next Article. IN BRIEF. Pathogenesis of Ulceration. Vascular Disease. Assessment of Diabetic Foot Ulcers.
Classification of Diabetic Foot Ulcers. Treatment Modalities. Article Navigation. Features April 01 A Review of the Pathophysiology, Classification, and Treatment of Foot Ulcers in Diabetic Patients Warren Clayton, Jr.
This Site. Google Scholar. Tom A. Elasy, MD, MPH Tom A. Elasy, MD, MPH.
Diabehic Herbal Tea Blends symptoms, like Herbal Tea Blends circulation and high blood Metabolism booster for men, can lead hlcers ulcers, especially on your criis. Proper foot ulcsrs can help to prevent crisjs from forming. Foot ulcers Hyperglycemic crisis and diabetic foot ulcers a common complication of diabetes that klcers not being managed through methods such as diet, exercise, and insulin treatment. Ulcers are formed as a result of skin tissue breaking down and exposing the layers underneath. All people with diabetes can develop foot ulcers, but good foot care can help prevent them. Treatment for diabetic foot ulcers varies depending on their causes. One of the first signs of a foot ulcer is drainage from your foot that might stain your socks or leak out in your shoe.Hyperglycemic crisis and diabetic foot ulcers -
Ruben Nieto knows firsthand that the only way to reduce your risk of those serious complications is to treat foot ulcers as soon as you detect signs of trouble.
Here, he explains the link between high blood sugar and foot ulcers and, most importantly, what you can do to prevent them. High blood glucose can cause sugar in your urine, and it can make you feel thirstier than normal.
High blood sugar can also lead to excessive hunger, vomiting, rapid heartbeat, and vision problems. Two of these long-term complications 一 nerve damage and poor circulation 一 explain the link between high blood glucose and foot ulcers.
Too much sugar in your blood can damage your nerves, and that includes the nerves in your feet. Nerve damage is particularly problematic because it can cause numbness. For example, you might cut your foot and not even realize it.
This can increase the time it takes for you to clean the wound and seek treatment. Nerve damage combined with poor circulation can lead to slow-healing wounds. Not only are diabetic wounds slow-healing, but diabetic neuropathy also negatively impacts your immune system, which means if you have a wound, your body has a harder time fighting off bacteria and other pathogens, which may lead to infection.
Scheduling routine diabetic foot care appointments allows Dr. Nieto to inspect your feet for any red flags as well as trim your nails and remove calluses. In addition to routine diabetic foot care, you can further reduce your risk of developing a foot ulcer by:.
When you have high blood sugar, poor circulation, and peripheral neuropathy, even the smallest tissue injury such as a small blister can become problematic. Without the adequate circulation to promote healing, small injuries can quickly become infected.
Diabetic wounds, including foot and leg ulcers, require immediate treatment. Also, visit your foot doctor every year more often if you have nerve damage for a complete exam, which will include checking for feeling and blood flow in your feet.
Keep the blood flowing. Choose feet-friendly activities like walking, riding a bike, or swimming. Check with your doctor about which activities are best for you and any you should avoid. See your regular doctor or foot doctor right away:.
Most people with diabetes can prevent serious foot complications. Skip directly to site content Skip directly to search. Español Other Languages. Diabetes and Your Feet.
Español Spanish. Minus Related Pages. Feeling No Pain Some people with nerve damage have numbness, tingling, or pain, but others have no symptoms. Amputation: What to Know. Read about how you can: Prevent diabetes-related amputations Recover from a diabetes-related amputation Care for your mental health after an amputation.
Could You Have Nerve Damage? Anyone with diabetes can develop nerve damage, but these factors increase your risk: Blood sugar levels that are hard to manage Having diabetes for a long time, especially if your blood sugar is often higher than your target levels Being overweight Being older than 40 years Having high blood pressure Having high cholesterol Nerve damage, along with poor blood flow—another diabetes complication—puts you at risk for developing a foot ulcer a sore or wound that could get infected and not heal well.
Smoking reduces blood flow to the feet. Follow a healthy eating plan , including eating more fruits and vegetables and less sugar and salt.
Get physically active —10 to 20 minutes a day is better than an hour once a week. Take medicines as prescribed by your doctor. Tips for Healthy Feet Get to the bottom of any foot problems by using a mirror or asking for help.
See your regular doctor or foot doctor right away: Pain in your legs or cramping in your buttocks, thighs, or calves during physical activity. Tingling, burning, or pain in your feet. Loss of sense of touch or ability to feel heat or cold very well. A change in the shape of your feet over time.
Loss of hair on your toes, feet, and lower legs. Dry, cracked skin on your feet. A change in the color and temperature of your feet. Thickened, yellow toenails. A blister, sore, ulcer, infected corn, or ingrown toenail. Tips for Healthy Feet infographic Diabetes Foot Problems: When to See Your Doctor infographic How Diabetes Can Affect Your Body Infographic Your Diabetes Care Schedule Diabetes Features CDC Diabetes on Facebook CDCDiabetes on Twitter.
Last Reviewed: April 11, Source: Centers for Disease Control and Prevention. Facebook Twitter LinkedIn Syndicate. home Diabetes Home.
Herbal Tea Blends Clayton, Jr. Elasy, MD, Hyperglycsmic, is medical Hyerglycemic of ffoot Vanderbilt Eskind Diabetes Center in the Division of Crisjs, Diabetes, and Metabolism Hyperglycemic crisis and diabetic foot ulcers Vanderbilt Astaxanthin and macular degeneration Medical Center in Nashville, Tenn. Elasy is editor-in-chief of Clinical Diabetes. Warren ClaytonTom A. Elasy; A Review of the Pathophysiology, Classification, and Treatment of Foot Ulcers in Diabetic Patients. Clin Diabetes 1 April ; 27 2 : 52— The development of lower extremity ulcers is a well known potential complication for patients with diabetes.Video
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Herbal Tea Blends all ulcers are infected; however, if your podiatric physician diagnoses an infection, a treatment program of antibiotics, wound care, and possibly hospitalization will be necessary.
These devices will reduce the pressure and irritation to the ulcer area and help to speed the healing process. The science of wound care has advanced significantly over the past ten years. We know that wounds and ulcers heal faster, with a lower risk of infection, if they are kept covered and moist.
The use of full-strength betadine, peroxide, whirlpools and soaking are not recommended, as this could lead to further complications. Appropriate wound management includes the use of dressings and topically-applied medications.
These range from normal saline to advanced products, such as growth factors, ulcer dressings, and skin substitutes that have been shown to be highly effective in healing foot ulcers. For a wound to heal there must be adequate circulation to the ulcerated area.
Your podiatrist may order evaluation test such as noninvasive studies and or consult a vascular surgeon. Tightly controlling blood glucose is of the utmost importance during the treatment of a diabetic foot ulcer.
Working closely with a medical doctor or endocrinologist to accomplish this will enhance healing and reduce the risk of complications. A majority of noninfected foot ulcers are treated without surgery; however, when this fails, surgical management may be appropriate.
Healing time depends on a variety of factors, such as wound size and location, pressure on the wound from walking or standing, swelling, circulation, blood glucose levels, wound care, and what is being applied to the wound.
Healing may occur within weeks or require several months. The best way to treat a diabetic foot ulcer is to prevent its development in the first place. Recommended guidelines include seeing a podiatrist on a regular basis. He or she can determine if you are at high risk for developing a foot ulcer and implement strategies for prevention.
Reducing additional risk factors, such as smoking, drinking alcohol, high cholesterol, and elevated blood glucose are important in the prevention and treatment of a diabetic foot ulcer.
Wearing the appropriate shoes and socks will go a long way in reducing risks. Your podiatric physician can provide guidance in selecting the proper shoes. Learning how to check your feet is crucial in noticing a potential problem as early as possible.
Inspect your feet every day—especially between the toes and the sole—for cuts, bruises, cracks, blisters, redness, ulcers, and any sign of abnormality. Each time you visit a health care provider, remove your shoes and socks so your feet can be examined. Adapted from APMA. Updated visitor policies.
Other Michigan Medicine Sites About Michigan Medicine UofMHealth. org Medical School Nursing Find a Clinical Trial. Frequently Asked Questions: Diabetic Foot Ulcers.
What Is a Diabetic Foot Ulcer? Who Can Get a Diabetic Foot Ulcer? How Do Diabetic Foot Ulcers Form? What Is the Value of Treating a Diabetic Foot Ulcer? Foot ulcers in patients with diabetes should be treated for several reasons: To reduce the risk of infection and amputation To improve function and quality of life To reduce health care costs How Should a Diabetic Foot Ulcer Be Treated?
Applying Medication and Dressings Appropriate wound management includes the use of dressings and topically-applied medications. Managing Blood Glucose Tightly controlling blood glucose is of the utmost importance during the treatment of a diabetic foot ulcer.
Surgical Options A majority of noninfected foot ulcers are treated without surgery; however, when this fails, surgical management may be appropriate. How Can a Foot Ulcer Be Prevented? You are at high risk if you: Have neuropathy Have poor circulation Have a foot deformity i.
bunion, hammer toe Wear inappropriate shoes Have uncontrolled blood sugar Reducing additional risk factors, such as smoking, drinking alcohol, high cholesterol, and elevated blood glucose are important in the prevention and treatment of a diabetic foot ulcer.
: Hyperglycemic crisis and diabetic foot ulcers| The Link Between High Blood Glucose and Foot Ulcers | Volume 46, Issue 1. An infection is a serious complication of a foot ulcer and requires immediate treatment. Gou W, Ling C-W, He Y, Jiang Z, Fu Y, Xu F, et al. l CrossRef Full Text Google Scholar. For further validation and comparison, we divided the patients in the training set into a survival group and a nonsurvival group according to their clinical outcomes and analysed the differences in features between the groups by statistical methods. Based on five representative machine learning algorithms, we trained prediction models on data from patients with hyperglycaemic crisis admitted to two tertiary hospitals between and Traditionally, linear models, such as logistic regression model and Cox proportional hazard model, have been used to develop such prediction models [ 8 , 9 , 10 , 11 , 12 ]. |
| ORIGINAL RESEARCH article | Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press. This content does not have an English version. This content does not have an Arabic version. Appointments at Mayo Clinic Mayo Clinic offers appointments in Arizona, Florida and Minnesota and at Mayo Clinic Health System locations. Request Appointment. Amputation and diabetes: How to protect your feet. Products and services. Amputation and diabetes: How to protect your feet Good diabetes management and regular foot care help prevent severe foot sores that are difficult to treat and may require amputation. By Mayo Clinic Staff. Thank you for subscribing! Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry. Show references Loscalzo J, et al. Diabetes mellitus: Complications In: Harrison's Principles of Internal Medicine. McGraw Hill; Accessed July 24, Matheson EM, et al. Diabetes-related foot infections: Diagnosis and treatment. American Family Physician. Retinopathy, neuropathy, and foot care: Standards of medical care in diabetes — Diabetes Care. Rossboth R, et al. Risk factors for diabetic foot complications in type 2 diabetes—A systematic review. Diabetes and foot problems. National Institute of Diabetes and Digestive and Kidney Diseases. What is a diabetic foot ulcer? American Podiatric Medical Association. Access July 24, Hingorani A, et al. The management of diabetic foot: A clinical practice guideline by the Society for Vascular Surgery in collaboration with the American Podiatric Medical Association and the Society for Vascular Medicine. Journal of Vascular Surgery. Weintrob AC, et al. Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities. Society for Vascular Surgery. Accessed June 21, Products and Services The Mayo Clinic Diet Online A Book: The Essential Diabetes Book. 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Using insulin Diabetic Gastroparesis Diuretics Diuretics: A cause of low potassium? Trauma Surgery. Our Locations. Patient Forms. Patient Resources. Patient Portal. Pay Bill Online. Patient Feedback. Medical Record Request. Clinical Trials. HIPAA Information. Financial Policy. Good Faith Estimate. Notice of Privacy. Chattanooga Surgical Foundation. The Diabetic Foot Crisis. Previous Next. WHAT CAN BE DONE? Share This Content! Facebook Twitter LinkedIn WhatsApp Tumblr Pinterest Email. Related Posts. New AV Fistula Creation Option for Chattanooga Dialysis Patients. December 27th, 0 Comments. Do You Need Compression Socks? December 2nd, 2 Comments. What You Need to Know About AAA. However, an insulin loading dose of 0. Multiple factors must be considered when titrating intravenous insulin continuous infusion 2. The rate of blood glucose reduction, insulin sensitivity, prandial coverage, and NPO status should all be taken into consideration 2. A rapid reduction in BG might be harmful and linked to cerebral edema 2. Moreover, the insulin infusion rate can be increased based on BG around major meals time and can be continued at a higher rate for hours following any major meal 2. Lastly, it is necessary to monitor BG among NPO patients closely. Randomized clinical trials compared the two strategies and found no difference 27 , Intravenous LD insulin administration has been associated with an increased risk of cerebral edema 27 , An acceptable alternative for patients with mild to moderate DKA could be a bolus of 0. Patients with end-stage renal disease ESRD and acute kidney injury AKI are considered a high-risk category that necessitates extra care 32 , To avoid rapid increases in osmolality and hypoglycemia in these patients; it is recommended that insulin infusions begin at 0. Subcutaneous insulin should overlap with intravenous insulin for at least minutes before its discontinuation to ensure the optimal transition of care 6 , A transition to subcutaneous long-acting insulin in addition to ultra-short acting insulin such as glargine and glulisine after resolution of DKA may result in reduced hypoglycemic events compared to other basal bolus regimens such as NPH insulin and insulin regular 24 , For newly diagnosed insulin-dependent diabetes patients, subcutaneous insulin may be started at a dose of 0. The transition process in patients who were previously using insulin or antidiabetic agents before to DKA admission is still unclear 24 , In ICU settings, clinicians tend to hold all oral antidiabetic agents and rely on insulin regimens for in-patient management given the shorter half-life of insulin and its predictability 24 , This could potentially be an area for further investigation on the transition process and its implication on patient outcomes 24 , Insulin sequestering to plastic IV tubing has been described, resulting in insulin wasting and dose inaccuracy 34 , Flushing the IV tube with a priming fluid of 20 mL is adequate to minimize the insulin losses to IV tube 34 , Patients with hyperglycemic crisiss are at a higher risk of developing hypokalemia due to multifactorial process 1 , Insulin therapy, correction of acidosis, and hydration all together lead to the development of hypokalemia 1 , Additionally, volume depletion seen with hyperglycemic crisis leads to secondary hyperaldosteronism, which exacerbates hypokalemia by enhancing urinary potassium excretion 1 , Serum potassium level should be obtained immediately upon presentation and prior to initiating insulin therapy 1 , Potassium replacement is required regardless of the baseline serum potassium level due to hydration and insulin therapy, except among renal failure patients 1 , It is suggested to administer 20 —30 mEq potassium in each liter of intravenous fluid to keep a serum potassium concentration within the normal range 1 , In addition to possible hypokalemia, patients with the hyperglycemic crisis could present with hypophosphatemia 1 , Osmotic diuresis during hyperglycemic crisis increases the urinary phosphate excretion, and insulin therapy enhances intracellular phosphate shift 1 , Phosphate replacement is not a fundamental part of hyperglycemic crisis management, given the lack of evidence of clinical benefit 1 , 29 , A special consideration with phosphate administration is the secondary hypocalcemia 1 , 29 , Acidemia associated with DKA results from the overproduction of ketoacids, generated from the haptic metabolism of free fatty acids. This hepatic metabolism occurs as a result of insulin resistance and an increase in the counterregulatory hormones contributing to the pathophysiology of DKA 37 , Tissue acidosis could lead to impaired myocardial contractility, systemic vasodilatation, inhibition of glucose utilization by insulin, and lowering the levels of 2,3-diphosphoglycerate 2,3-DPG in erythrocytes 37 — Sodium bicarbonate decreases the hemoglobin-oxygen affinity leading to tissue hypoxia; moreover, it is associated with hypernatremia, hypocalcemia, hypokalemia, hypercapnia, prolonged QTc interval, intracellular acidosis, and metabolic alkalosis 39 , The use of adjuvant sodium bicarbonate in the setting of DKA consistently shows a lack of clinical benefit and should be prescribed on a case-by-case basis. Although this recommendation was not supported by solid evidence; many clinicians adopt the practice to avoid the unwanted side effect of severe metabolic acidosis. Sodium bicarbonate moves potassium intracellularly, however, clinical benefit is uncertain, and the use is controversial 41 , Prompt therapy for patients with hyperglycemic crisis is essential in reducing morbidity and mortality 6 , If not treated or treated ineffectively, the prognosis can include serious complications such as seizures, organ failures, coma, and death 6 , When treatment is delayed, the overall mortality rate of HHS is higher than that of DKA, especially in older patients. This difference in prognoses was comparable when patients were matched for age In DKA, prolonged hypotension can lead to acute myocardial and bowel infarction 6 , The kidney plays a vital role in normalizing massive pH and electrolyte abnormalities 6 , Patients with prior kidney dysfunction or patients who developed end-stage chronic kidney disease worsen the prognosis considerably 6 , In HHS, severe dehydration may predispose the patient to complications such as myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation 6 , The VTE risk was higher than diabetic patients without hyperglycemic crisis or diabetic acidosis patients Management of hyperglycemic crisis may also be associated with significant complications include electrolyte abnormalities, hypoglycemia, and cerebral edema 7. This is due to the use of insulin and fluid replacement therapy 4 , 5. Therefore, frequent electrolytes and blood glucose concentrations monitoring are essential while insulin infusions and fluid replacements are continued 4 , 5. Cerebral edema is a rare but severe complication in children and adolescents and rarely affects adult patients older than 28 7. This could be due to the lack of cerebral autoregulation, presentation with more severe acidosis and dehydration among children and adolescents The exact mechanism of cerebral edema development is unknown. Some reports suggest that the risk of cerebral edema during hyperglycemic crisis management might be induced by rapid hydration, especially in the pediatric population. However, a recent multicenter study for children with DKA who were randomized to receive isotonic versus hypotonic sodium IV fluid with different infusions rates did not show a difference in neurological outcomes Early identification and prompt therapy with mannitol or hypertonic saline can prevent neurological deterioration from DKA management 7 , Furthermore, higher blood urea nitrogen BUN and sodium concentrations have been identified as cerebral edema risk factors Thus, careful hydration with close electrolytes and BUN is recommended Other serious complications of hyperglycemic crisis may include transient AKI, pulmonary edema in patients with congestive heart failure, myocardial infarction, a rise in pancreatic enzymes with or without acute pancreatitis, cardiomyopathy, rhabdomyolysis in patients presented with severe dehydration 7 , All authors have contributed equally in writing, organizing, and reviewing this publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 32 7 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Goyal A, Mathew UE, Golla KK, Mannar V, Kubihal S, Gupta Y, et al. A Practical Guidance on the Use of Intravenous Insulin Infusion for Management of Inpatient Hyperglycemia. Diabetes Metab Syndrome: Clin Res Rev 15 5 CrossRef Full Text Google Scholar. Saeedi P. Global and Regional Diabetes Prevalence Estimates for and Projections for and Results From the International Diabetes Federation Diabetes Atlas, 9th Edition. Diabetes Res Clin Pract Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment. Dia Care 37 11 — Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Management of Hyperglycemic Crises in Patients With Diabetes. Diabetes Care 24 1 — Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic Crises in Adult Patients With Diabetes: A Consensus Statement From the American Diabetes Association. Diabetes Care 29 12 — Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome: Review of Acute Decompensated Diabetes in Adult Patients. BMJ I Fayfman M, Pasquel FJ, Umpierrez GE. Management of Hyperglycemic Crises. Med Clinics North Am 3 — Rains JL, Jain SK. Oxidative Stress, Insulin Signaling, and Diabetes. Free Radical Biol Med 50 5 — Hoffman WH, Burek CL, Waller JL, Fisher LE, Khichi M, Mellick LB. Cytokine Response to Diabetic Ketoacidosis and Its Treatment. Clin Immunol 3 — Hayami T, Kato Y, Kamiya H, Kondo M, Naito E, Sugiura Y, et al. Case of Ketoacidosis by a Sodium-Glucose Cotransporter 2 Inhibitor in a Diabetic Patient With a Low-Carbohydrate Diet. J Diabetes Investig , 6 5 — Umpierrez GE, Murphy MB, Kitabchi AE. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome. Diabetes Spectr 15 1 Kraut JA, Madias NE. Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. |
| Diabetes and Your Feet | Nerve damage can also lower your ability to feel pain, heat, or cold. Living without pain sounds pretty good, but it comes at a high cost. Read about how you can:. Nerve damage, along with poor blood flow—another diabetes complication—puts you at risk for developing a foot ulcer a sore or wound that could get infected and not heal well. When you check your feet every day, you can catch problems early and get them treated right away. Early treatment greatly reduces your risk of amputation. Keep your blood sugar in your target range as much as possible. This is one of the most important things you can do to prevent nerve damage or stop it from getting worse. Other good diabetes management habits can help, too:. Check your feet every day for cuts, redness, swelling, sores, blisters, corns, calluses, or any other change to the skin or nails. Wash your feet every day in warm not hot water. Dry your feet completely and apply lotion to the top and bottom—but not between your toes, which could lead to infection. Never go barefoot. Always wear shoes and socks or slippers, even inside, to avoid injury. Wear shoes that fit well. For the best fit, try on new shoes at the end of the day when your feet tend to be largest. Always wear socks with your shoes. Trim your toenails straight across and gently smooth any sharp edges with a nail file. Get your feet checked at every health care visit. Also, visit your foot doctor every year more often if you have nerve damage for a complete exam, which will include checking for feeling and blood flow in your feet. Keep the blood flowing. Choose feet-friendly activities like walking, riding a bike, or swimming. Check with your doctor about which activities are best for you and any you should avoid. See your regular doctor or foot doctor right away:. Most people with diabetes can prevent serious foot complications. Skip directly to site content Skip directly to search. Español Other Languages. Diabetes and Your Feet. Español Spanish. Minus Related Pages. Feeling No Pain Some people with nerve damage have numbness, tingling, or pain, but others have no symptoms. Amputation: What to Know. Read about how you can: Prevent diabetes-related amputations Recover from a diabetes-related amputation Care for your mental health after an amputation. Could You Have Nerve Damage? DM remains a leading cause of death worldwide and is the number one cause of kidney failure, lower-limb amputations, and adult blindness 1 , 3 , 4. The global prevalence of DM in was around 9. Due to this high prevalence of DM, emergency admissions for hyperglycemic crisis, Diabetic Ketoacidosis DKA and Hyperglycemic Hyperosmolar State HHS , still very common and challenging 1 — 3. Both conditions have high mortality rates if kept not treated. However, higher mortality rates were reported among elderly patients diagnosed with DKA 1. DKA and HHS have similar pathophysiology with some differences. The pathogenesis behind HHS is not as well understood 2 , 5. DKA is a complex metabolic disorder caused by an absolute or relative effective insulin concentration reduction and increased in catecholamines, cortisol, glucagon, and growth hormones 5 , 6. Hyperglycemia is explained by three main mechanisms: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues 7. Insulin reduction and increased counterregulatory hormones in DKA accelerate the lipolysis, which results in the release of free fatty acids into the circulation from adipose tissue and stimulates the conversion of fatty acid to ketone by liver oxidation 7 , 8. This profound increase in free fatty acid and ketone concentrations lead to a further increase in the magnitude of hyperglycemia by inducing insulin resistance and ultimately results in ketonemia and metabolic acidosis 7 , 8. Previous studies have shown that excessive glucose levels and fatty acids are associated with a pro-inflammatory and oxidative state among DKA patients 9 , Oxidative stress is defined as an increase in reactive oxygen species ROS generation 9. Overproduction of ROS results in cellular damage of lipids, membranes, and proteins 9. Additionally, the oxidative state increases the risk of developing chronic diabetic complications following the DKA event 9. Significant increase of IL-6, -1B and -8, and TNF-α and other cytokines reduce the response to insulin therapy. Insulin therapy and hydration are essential in normalizing these parameters 9. In contrast to DKA, insulin production is not significantly reduced among HHS patients 4. This minimal insulin production is adequate to prevent lipolysis and ketogenesis 4 , 5. HHS is characterized by severe elevations in serum glucose concentrations and hyperosmolality 4 , 5. This extreme elevation in serum hyperosmolality results in osmotic diuresis, a greater degree of dehydration, and more fluid loss than DKA 4 , 5. This significant loss of intracellular fluids results in much higher blood glucose BG with HHS in comparison to DKA 4 , 5. Euglycemic DKA is another unique presentation of DKA and has been reported more often recently 6 , Euglycemic DKA has been linked with many factors, such as treatment of diabetes, carbohydrate restriction, high alcohol intake, and inhibition of gluconeogenesis 6 , It also can be induced due to certain medications, most commonly seen with sodium-glucose cotransporter 2 SGLT-2 inhibitors and insulin 6 , DKA develops more rapidly in comparison to HHS. In some cases, it only takes a few hours from the precipitating factor for DKA to develop Both metabolic disorders present with classical hyperglycemia symptoms: polyuria, polydipsia, weakness, and mental status changes 6 , Additionally, patients with HHS and DKA often present with signs of dehydration, such as dry mucous membranes, poor skin turgor, tachycardia, hypotension, and increased capillary refill with severe dehydration 8 , If DKA worsens and is left without treatment, it can eventually lead to unconsciousness 6. The initial laboratory assessment of patients with suspected DKA or HHS should include BG, blood urea nitrogen, serum creatinine, serum ketones, electrolytes, anion gap, osmolality, urine ketones, and arterial blood gases 6 , 8. Other reasons for high anion gap metabolic acidosis, such as ethyl glycol toxicity, isoniazid overdose, lactic acidosis, methanol toxicity, propylene glycol ingestion, salicylates toxicity, and uremia, must be ruled out Diagnostic criteria for DKA and HHS are listed in Table 1 6. Patients with a higher level of osmolarity and pH present with worse dehydration and mental status 4. DKA resolution is achieved following the correction of dehydration, hyperglycemia, and electrolyte imbalances 2 , 6 , 8. In addition to the previously mentioned criteria, normal osmolality is required for HHS resolution 6 , 8. Figure 1 displays a suggested management pathway of DKA and HHS based on the American Diabetes Association ADA guidelines and Joint British Diabetes Societies for Inpatient Care JBDS-IP revised guidelines 1 , Figure 1 Pathway displays the management of diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS. Fluid therapy is a cornerstone for the management of DKA and HHS. Aggressive repletion with isotonic saline expands the extracellular volume and stabilizes cardiovascular functions The initial fluid management general practice and protocols are based on the ADA guidelines statement for the management of hyperglycemic crises in adult patients with diabetes 1. It recommends initiating 0. Half normal saline 0. During fluid replacement, it is expected that hyperglycemia will be corrected faster than ketoacidosis and DKA resolution 1. Appropriate assessment of serum osmolality, urine output, and cardiac function should be performed to guide the aggressive fluid administration and avoid iatrogenic overload 1. However, optimal initial fluid therapy for managing DKA or HHS was not evident by clinical trials to evaluate the efficacy and safety outcomes of using normal saline or other crystalloid 1. It is known that using 0. Some practitioners may use balanced fluids as an alternative to overcome this side effect, as its different composition could physiologically lead to a faster resolution of acidosis Common types of crystalloid IV fluids and their composition are listed in Table 2 Small trials evaluated the effect of balanced fluids and 0. They found that balanced crystalloids significantly resulted with a shorter median time for DKA resolution than saline At the same time, it significantly led to a shorter median time for insulin discontinuation than saline 9. They found no significant difference in DKA resolution at 48 hours, ICU, and hospital length of stay. However, PL group had significantly reached more DKA resolution at 24 hours in comparison to 0. In conclusion, designing an appropriate fluid repletion therapy for DKA and HHS management will need careful planning and monitoring for choosing the appropriate fluid type, volume, and rate for the patient. Insulin is considered to be one of the three fundamental elements of DKA and HHS management 2 , 6 , It reduces hepatic glucose synthesis, enhances peripheral glucose utilization, and inhibits lipolysis, ketogenesis, and glucagon secretion, lowering plasma glucose levels and decreasing ketone bodies production 6 , Insulin should be given immediately after the initial fluid resuscitation 2 , 6 , The aim of using insulin in DKA and HHS is to close the anion gap generated by the production of ketone bodies rather than aiming for euglycemia 6 , Intravenous administration of insulin regular mixed in NaCl 0. Insulin can also be used as frequent subcutaneous or intramuscular injections for the treatment of DKA in mild-moderate DKA patients 6 , However, a continuous intravenous insulin regimen is preferred over subcutaneous insulin for DKA management overall due to its short half-life, fast onset, and easy titration 6 , The use of basal insulin analogs in conjunction with regular insulin infusions may speed up the resolution of DKA and minimize rebound hyperglycemia events, resulting in less ICU length of stay and less healthcare cost 6 , Insulin is currently recommended as a continuous infusion at 0. Insulin loading dose has been linked to increasing the risk of cerebral edema and worsening shock Thus, insulin loading dose should be avoided at the beginning of therapy However, an insulin loading dose of 0. Multiple factors must be considered when titrating intravenous insulin continuous infusion 2. The rate of blood glucose reduction, insulin sensitivity, prandial coverage, and NPO status should all be taken into consideration 2. A rapid reduction in BG might be harmful and linked to cerebral edema 2. Moreover, the insulin infusion rate can be increased based on BG around major meals time and can be continued at a higher rate for hours following any major meal 2. Lastly, it is necessary to monitor BG among NPO patients closely. Randomized clinical trials compared the two strategies and found no difference 27 , Intravenous LD insulin administration has been associated with an increased risk of cerebral edema 27 , An acceptable alternative for patients with mild to moderate DKA could be a bolus of 0. Patients with end-stage renal disease ESRD and acute kidney injury AKI are considered a high-risk category that necessitates extra care 32 , To avoid rapid increases in osmolality and hypoglycemia in these patients; it is recommended that insulin infusions begin at 0. Subcutaneous insulin should overlap with intravenous insulin for at least minutes before its discontinuation to ensure the optimal transition of care 6 , A transition to subcutaneous long-acting insulin in addition to ultra-short acting insulin such as glargine and glulisine after resolution of DKA may result in reduced hypoglycemic events compared to other basal bolus regimens such as NPH insulin and insulin regular 24 , For newly diagnosed insulin-dependent diabetes patients, subcutaneous insulin may be started at a dose of 0. The transition process in patients who were previously using insulin or antidiabetic agents before to DKA admission is still unclear 24 , In ICU settings, clinicians tend to hold all oral antidiabetic agents and rely on insulin regimens for in-patient management given the shorter half-life of insulin and its predictability 24 , This could potentially be an area for further investigation on the transition process and its implication on patient outcomes 24 , Insulin sequestering to plastic IV tubing has been described, resulting in insulin wasting and dose inaccuracy 34 , Flushing the IV tube with a priming fluid of 20 mL is adequate to minimize the insulin losses to IV tube 34 , Patients with hyperglycemic crisiss are at a higher risk of developing hypokalemia due to multifactorial process 1 , Insulin therapy, correction of acidosis, and hydration all together lead to the development of hypokalemia 1 , Additionally, volume depletion seen with hyperglycemic crisis leads to secondary hyperaldosteronism, which exacerbates hypokalemia by enhancing urinary potassium excretion 1 , Serum potassium level should be obtained immediately upon presentation and prior to initiating insulin therapy 1 , Potassium replacement is required regardless of the baseline serum potassium level due to hydration and insulin therapy, except among renal failure patients 1 , It is suggested to administer 20 —30 mEq potassium in each liter of intravenous fluid to keep a serum potassium concentration within the normal range 1 , In addition to possible hypokalemia, patients with the hyperglycemic crisis could present with hypophosphatemia 1 , Osmotic diuresis during hyperglycemic crisis increases the urinary phosphate excretion, and insulin therapy enhances intracellular phosphate shift 1 , Phosphate replacement is not a fundamental part of hyperglycemic crisis management, given the lack of evidence of clinical benefit 1 , 29 , A special consideration with phosphate administration is the secondary hypocalcemia 1 , 29 , Acidemia associated with DKA results from the overproduction of ketoacids, generated from the haptic metabolism of free fatty acids. This hepatic metabolism occurs as a result of insulin resistance and an increase in the counterregulatory hormones contributing to the pathophysiology of DKA 37 , Tissue acidosis could lead to impaired myocardial contractility, systemic vasodilatation, inhibition of glucose utilization by insulin, and lowering the levels of 2,3-diphosphoglycerate 2,3-DPG in erythrocytes 37 — Sodium bicarbonate decreases the hemoglobin-oxygen affinity leading to tissue hypoxia; moreover, it is associated with hypernatremia, hypocalcemia, hypokalemia, hypercapnia, prolonged QTc interval, intracellular acidosis, and metabolic alkalosis 39 , The use of adjuvant sodium bicarbonate in the setting of DKA consistently shows a lack of clinical benefit and should be prescribed on a case-by-case basis. Although this recommendation was not supported by solid evidence; many clinicians adopt the practice to avoid the unwanted side effect of severe metabolic acidosis. Sodium bicarbonate moves potassium intracellularly, however, clinical benefit is uncertain, and the use is controversial 41 , Prompt therapy for patients with hyperglycemic crisis is essential in reducing morbidity and mortality 6 , If not treated or treated ineffectively, the prognosis can include serious complications such as seizures, organ failures, coma, and death 6 , When treatment is delayed, the overall mortality rate of HHS is higher than that of DKA, especially in older patients. This difference in prognoses was comparable when patients were matched for age In DKA, prolonged hypotension can lead to acute myocardial and bowel infarction 6 , The kidney plays a vital role in normalizing massive pH and electrolyte abnormalities 6 , Patients with prior kidney dysfunction or patients who developed end-stage chronic kidney disease worsen the prognosis considerably 6 , In HHS, severe dehydration may predispose the patient to complications such as myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation 6 , The VTE risk was higher than diabetic patients without hyperglycemic crisis or diabetic acidosis patients Management of hyperglycemic crisis may also be associated with significant complications include electrolyte abnormalities, hypoglycemia, and cerebral edema 7. This is due to the use of insulin and fluid replacement therapy 4 , 5. Therefore, frequent electrolytes and blood glucose concentrations monitoring are essential while insulin infusions and fluid replacements are continued 4 , 5. Cerebral edema is a rare but severe complication in children and adolescents and rarely affects adult patients older than 28 7. This could be due to the lack of cerebral autoregulation, presentation with more severe acidosis and dehydration among children and adolescents The exact mechanism of cerebral edema development is unknown. Some reports suggest that the risk of cerebral edema during hyperglycemic crisis management might be induced by rapid hydration, especially in the pediatric population. However, a recent multicenter study for children with DKA who were randomized to receive isotonic versus hypotonic sodium IV fluid with different infusions rates did not show a difference in neurological outcomes Early identification and prompt therapy with mannitol or hypertonic saline can prevent neurological deterioration from DKA management 7 , Furthermore, higher blood urea nitrogen BUN and sodium concentrations have been identified as cerebral edema risk factors Thus, careful hydration with close electrolytes and BUN is recommended Other serious complications of hyperglycemic crisis may include transient AKI, pulmonary edema in patients with congestive heart failure, myocardial infarction, a rise in pancreatic enzymes with or without acute pancreatitis, cardiomyopathy, rhabdomyolysis in patients presented with severe dehydration 7 , All authors have contributed equally in writing, organizing, and reviewing this publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 32 7 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Goyal A, Mathew UE, Golla KK, Mannar V, Kubihal S, Gupta Y, et al. A Practical Guidance on the Use of Intravenous Insulin Infusion for Management of Inpatient Hyperglycemia. Diabetes Metab Syndrome: Clin Res Rev 15 5 CrossRef Full Text Google Scholar. Saeedi P. Global and Regional Diabetes Prevalence Estimates for and Projections for and Results From the International Diabetes Federation Diabetes Atlas, 9th Edition. Diabetes Res Clin Pract Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment. Dia Care 37 11 — Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Management of Hyperglycemic Crises in Patients With Diabetes. Diabetes Care 24 1 — Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic Crises in Adult Patients With Diabetes: A Consensus Statement From the American Diabetes Association. Diabetes Care 29 12 — Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome: Review of Acute Decompensated Diabetes in Adult Patients. BMJ I Fayfman M, Pasquel FJ, Umpierrez GE. Management of Hyperglycemic Crises. |
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