Hyperglycaemic crises and lactic acidosis in diabetes mellitus

Abstract

Diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and lactic acidosis represent three of the most serious acute complications of diabetes. There have been some advances in our understanding of the pathogenesis of these conditions over the last three decades, together with more uniform agreement on their treatment and innovations in technology. Accordingly their incidence, morbidity, and mortality are decreasing, but at rates that fall short of our aspirations. Hyperglycaemic crises in particular remain an important cause of morbidity and mortality in diabetic populations around the world. In this article, understanding of these conditions and advances in their management, and the available guidelines for their treatment, are reviewed. As far as is possible, the recommendations are based on clear published evidence; failing that, what is considered to be a common sense synthesis of consensus guidelines and recommendations is provided.

Principles of Quantitative Fluid and Cation Replacement in Extreme Hyperglycemia

“…Even at normal body weight, the margin of error of the anthropometric formulas estimating body water is in the order of a few liters. Used in subjects with substantial water deficits, these formulas systematically overestimate body water [61][62][63][64]. This was our reason for basing the estimates of body water on the normal euglycemic state in this report.…”

Oxytocin Receptor Gene Polymorphisms in Patients With Diabetes

“…The OXTR gene, located on chromosome 3, is composed of four exons and three introns. The OXTR gene product is a transmembrane chain of seven domains, belonging to class 1 G proteins (31). Previous obtained data have shown that OXTR activity is necessary for a variety of processes; for example, in the Prader-Willi syndrome, there are deficits of OXT in neurons, while experimental OXTR-deficient animal models show hyperphagia and an increased meal size (32)(33)(34).…”

Managing hyperglycaemic emergencies: an illustrative case and review of recent British guidelines

“…In DKA, the lack of insulin combined with increased catecholamine levels leads to lipolysis, fatty acid production and ketogenesis; whereas in HHS, residual beta-cell function is sufficient to prevent lipolysis but not hyperglycaemia. 1 The main difference between the clinical presentations of DKA and HHS is that the former usually presents acutely, whereas the latter has a more subacute presentation. 2 Other differences in presentation have been suggested by the American Diabetes Association (Table 1).…”