Epidemiologic studies show that glucose control in hospitals is woefully inadequate.
Approximately 30% of hospitalized patients have blood glucose values >180 mg/dL.
Hyperglycemia and insulin regulation play both a direct and indirect role in the cellular mechanisms underlying inflammation and oxidative stress.
Free fatty acids generated by hyperglycemia and insulin deficiency also result in endothelial dysfunction and the generation of reactive oxygen species.
Diabetes is an increasingly prevalent diagnosis among hospitalized patients.
Many patients have unrecognized diabetes.
Diabetes contributes to greater lengths of stay and increased costs among hospitalized patients.
Identifying and treating diabetes:
Hyperglycemia is common in critically ill patients, both with and without diabetes.
Hyperglycemia is a predictor of adverse outcomes, including mortality.
Hyperglycemia is associated with poor outcomes in noncritically ill patients.
Glycemic goals for noncritically ill patients
Premeal blood glucose: <140 mg/dL
Random blood glucose: <180 mg/dL
DKA and HHS are life-threatening emergencies.
Attention to precipitating cause
Fluid and electrolyte management
Prevention of metabolic complications during recovery
Hyperglycemia is associated with adverse clinical outcomes in the hospital setting, both in critically ill and noncritically ill patients.
National organizations have promoted safe and achievable glucose targets for inpatients.
Special considerations are necessary for patients
Various patient- and provider-specific factors may increase the risk of inpatient hypoglycemia
Hypoglycemia is costly
- Patient level: increases risk of complications
- Institutional level: increases cost of care and may reduce reimbursement (Medicare “never” event)
Insulin is the most appropriate agent for the majority of hospitalized patients.
Insulin is a “high-alert medication.”
For effective and safe use of insulin, institutions need to consider
Standardized pharmacy operations
Education of nursing and support staff
Nurses are essential—and central—to successful implementation of protocols, order sets, glucose monitoring, and educational programs to support improved glycemic control.
The last 18 hours in utero have a significant impact on the infant’s metabolic responses after birth, even if maternal glucose control is adequate over the duration of gestation.
Hyperglycemia in the hospital affects quality of care, patient safety, length of stay, and cost; hence, addressing hyperglycemia in hospitalized patients can unite professionals in a common quest.
Models for implementation of improved control of hyperglycemia include:
Glucometrics is a way to measure the success of inpatient glucose management. Getting timely and accurate metrics to frontline clinical teams, which can analyze the results and look for cause and effect, will transform performance improvement into optimal outcomes.
Glucometrics generally consists of 3 measures:
Upon admission (or as soon thereafter as possible), every patient’s need for diabetes education should be assessed.
During hospital stay, all patients with diabetes should receive necessary training in diabetes knowledge and self-care skills.
Obesity is a neuroendocrine disease that is itself associated with numerous metabolic and biomechanical complications. It is generally defined as a body mass index (BMI) ≥30 kg/m2, especially in the presence of obesity-related complications. In the context of prediabetes, obesity (1-3):
The primary goal of prediabetes management is to normalize glucose levels and prevent or delay progression to diabetes and associated microvascular complications (1,2). Management of common prediabetes comorbidities such as obesity, hypertension, dyslipidemia, cardiovascular disease, and chronic kidney disease is also essential.
Diabetes affects 9.4% of the population of the United States, or approximately 30.3 million people. Of these, 7.2 million have not been diagnosed. Approximately 90% of all diabetes cases are type 2 diabetes.1
Patients with type 1 diabetes (T1D) require exogenous insulin for survival and should be identified as soon as possible to avoid high morbidity due to a delay in insulin treatment.
The risk factors for the development of both prediabetes and type 2 diabetes mellitus (T2DM) are as follows:1
There is a continuum of risk for poor patient outcomes as glucose tolerance progresses from normal to overt type 2 diabetes.
The Comprehensive Care Plan
Epidemiologic data have demonstrated significant increases of various cancers in people with obesity and diabetes. Recently, concern has emerged that antihyperglycemic medications may also be associated with an increased prevalence of multiple cancers; however, available data are limited and conflicting.1,2
Comprehensive care of patients with diabetes requires a team of healthcare professionals. Working with different healthcare providers allows the patient to learn in-depth information regarding their health and well-being. It also ensures that the patient’s needs are cared for and addressed.
GDM Definition, Etiology, Risk Factors, and Pathophysiology
AACE recommends that individuals who meet any of the clinical risk criteria noted below should be screened for prediabetes or type 2 diabetes (T2D)1.
Type 1 diabetes (T1D) is a chronic autoimmune disorder that occurs in genetically susceptible individuals and that may be precipitated by environmental factors. In a susceptible individual, the immune system is triggered to develop an autoimmune response against altered pancreatic beta cell antigens, or molecules in beta cells that resemble a viral protein.
Optimal management of type 2 diabetes requires treatment of the “ABCs” of diabetes: A1C, blood pressure, and cholesterol (ie, dyslipidemia). This web page provides the rationale and targets for glucose management; AACE guidelines for blood pressure and lipid control are summarized in Management of Common Comorbidities of Diabetes.
As may be expected with a chronic disease that primarily affects middle-aged and older individuals, type 2 diabetes is usually complicated by other medical conditions.
What impact does intensive blood glucose control have on CV complications in patients with diabetes? What are the major findings of CV outcome trials conducted the past 10 years? Does intensive glucose control improve CV mortality? What are important considerations for future studies?
What are the main objectives of the cardiovascular outcomes trials (CVOT) for type 2 diabetes (T2D) therapeutics? Over the past 7 years, what have the outcomes of major CVOTs for T2D therapeutics shown? Which drug classes have demonstrated the greatest cardiovascular benefits? How have diabetes guidelines changed in response to results of CVOT trials?
How is ASCVD risk assessed? What are the benefits and disadvantages of the various available risk assessment tools? Is metabolic syndrome a stronger predictor of CV risk compared to CV risk scoring tools? How do emerging risk markers further refine risk stratification?
The Cholesterol Hypothesis, also known as the Lipid Hypothesis, postulates a direct link between blood cholesterol levels and CHD. Studies show a higher and earlier occurrence of heart disease in patients with higher blood lipid levels. Strategies to decrease plasma lipid levels (primarily LDL - C) reduces CHD risk at the patient and population level. Although other CHD risk factors exist, the causal role of lipid accumulation in CHD pathogenesis has been shown in clinical, epidemiologic, and genetic analyses. Based on the strength of available evidence, is it time to rename the “Cholesterol Hypothesis” the “Cholesterol Principle”?
What are the types and key features of triglyceride - rich lipoproteins (T G RLs)? What are the endogenous and exogenous metabolic pathways of T G RLs ? What is the role of polymorphisms in metabolic abnormalities of triglycerides? What role do T G RLs play in atherosclerotic cardiovascular disease (ASCVD)?
What is nico7nic acid (niacin)? What are the recognized side effects of niacin? What are the key results from clinical and imaging trials of niacin treatment? How did results from “historical” trials differ from results of the more “recent” AIM - HIGH and HPS2 - THRIVE RCTs, and how did trial designs differ?
What is the role of statin therapy in the management of dyslipidemia and prevention of CVD? What are starting statin doses, dosage ranges, metabolic effects, and main considerations? How should statin treatment be monitored? What is the major evidence supporting the use of statin therapy?
What risk factors contribute to a patient's total risk profile for cardiometabolic disease, including residual CAD risk? How does targeting HDL - C vs HDL - P affect risk? What are the merits of targeting (reducing) TG and how does the setting of high cholesterol contribute to risk associated with high TGs? What are the benefits of lowering LDL - C, non - HDL - C, Apo B, and LDL - P? How low should LDL - C lowering go?
What are proprotein convertase subtilisin/ kexin type 9 ( PCSK9) inhibitors and how do they work? Which patients are candidates for PCSK9 inhibitor therapy? What is the expected response to PCSK9 inhibitor therapy?
What have recent studies shown regarding residual CV risk in patients on statins? What new agents are available to address residual risk? What are the mechanisms of action of these therapeutics, and what patient populations do they benefit? What are current AACE recommendations for the use of novel new therapeutic agents for ASCVD?
What is the risk burden of hypertriglyceridemia? What is the clinical and gene7c evidence for the associa7on between elevated TG and atherosclerosis? What are the evidence - based guideline recommenda7ons for managing pa7ents with hypertriglyceridemia? What TG - lowering agents are available, and what are their an7 - atherosclero7c and an7 - inflammatory proper7es?
What are the causes of dyslipidemia? What are current lipid treatment goals? What treatments are available for dyslipidemia? How should treatment be monitored?
What is the role of fibrates in the treatment of dyslipidemia? What key studies have demonstrated significant clinical benefit with combination therapy (statins + fibrates)? What are the current AACE treatment guidelines regarding the use of fibrates for dyslipidemia management? What specific populations benefit from fibrate therapy?
What are omega - 3 fatty acids/fish oil and how do they fit into treatment for dyslipidemia? What are the recommendations and considerations for treatment with omega - 3 fatty acids/fish oil?
What dietary factors increase the risk of CVD? What is the place of nutrition in reducing the risk of CVD and improving cardiovascular health in patients with dyslipidemia? How do different nutrients contribute to improving CVD health?
CANTOS and JUPITER Studies
What is familial chylomicronemia syndrome (FCS) and how does it differ from other types of severe HTG? What is the pathophysiology of severe HTG and FCS? What are the adverse consequences of severe HTG (with or without FCS) and what is their pathophysiology? How should FCS be diagnosed? How should FCS be management?
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