Health Care Utilization and Burden of Diabetic Ketoacidosis in the U.S. Over the Past Decade: A Nationwide Analysis

The American "stroke belt" has contributed to the study of stroke. However, U.S. geographic patterns of diabetes have not been as specifically characterized. This study identifies a geographically coherent region of the U.S. where the prevalence of diagnosed diabetes is especially high, called the "diabetes belt." In 2010, data from the 2007 and 2008 Behavioral Risk Factor Surveillance System were combined with county-level diagnosed diabetes prevalence estimates. Counties in close proximity with an estimated prevalence of diagnosed diabetes ≥11.0% were considered to define the diabetes belt. Prevalence of risk factors in the diabetes belt was compared to that in the rest of the U.S. The fraction of the excess risk associated with living in the diabetes belt associated with selected risk factors, both modifiable (sedentary lifestyle, obesity) and nonmodifiable (age, gender, race/ethnicity, education), was calculated. A diabetes belt consisting of 644 counties in 15 mostly southern states was identified. People in the diabetes belt were more likely to be non-Hispanic African-American, lead a sedentary lifestyle, and be obese than in the rest of the U.S. Thirty percent of the excess risk was associated with modifiable risk factors, and 37% with nonmodifiable factors. Nearly one third of the difference in diabetes prevalence between the diabetes belt and the rest of the U.S. is associated with sedentary lifestyle and obesity. Culturally appropriate interventions aimed at decreasing obesity and sedentary lifestyle in counties within the diabetes belt should be considered. Published by Elsevier Inc.

The prognosis of diabetic ketoacidosis has undergone incredibly remarkable evolution since the discovery of insulin nearly a century ago. The incidence and economic burden of diabetic ketoacidosis have continued to rise but its mortality has decreased to less than 1% in good centers. Improved outcome is attributable to a better understanding of the pathophysiology of the disease and widespread application of treatment guidelines. In this review, we present the changes that have occurred over the years, highlighting the evidence behind the recommendations that have improved outcome. We begin with a discussion of the precipitants and pathogenesis of DKA as a prelude to understanding the rationale for the recommendations. A brief review of ketosis-prone type 2 diabetes, an update relating to the diagnosis of DKA and a future perspective are also provided.

Several investigators have reported that more than half of African-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic features of type 2 diabetes during follow-up. These patients are usually obese, have a strong family history of diabetes, have a low prevalence of autoimmune markers, and lack a genetic association with HLA. Their initial presentation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating cause of metabolic decompensation. At presentation, they have markedly impaired insulin secretion and insulin action, but intensified diabetic management results in significant improvement in beta-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of follow-up. On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. The absence of autoimmune markers and the presence of measurable insulin secretion have proven useful in predicting near-normoglycemic remission and long-term insulin dependence in adult patients with a history of diabetic ketoacidosis. This clinical presentation is commonly reported in African and African-American persons but is also observed in Hispanic persons and those from other minority ethnic groups. The underlying mechanisms for beta-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, preliminary evidence suggests an increased susceptibility to glucose desensitization.