Abstract
Hyperglycaemia occurs frequently in the critically ill, even in those patients without a history of diabetes. The mechanisms underlying hyperglycaemia in this group are complex and incompletely defined. In health, the gastrointestinal tract is an important modulator of postprandial glycaemic excursions and both the rate of gastric emptying and the so-called incretin hormones, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, are pivotal determinants of postprandial glycaemia. Incretin-based therapies (that is, glucagon-like peptide-1 agonists and dipeptidyl-peptidase-4 inhibitors) have recently been incorporated into standard algorithms for the management of hyperglycaemia in ambulant patients with type 2 diabetes and, inevitably, an increasing number of patients who were receiving these classes of drugs prior to their acute illness will present to ICUs. This paper summarises current knowledge of the incretin effect as well as the incretin-based therapies that are available for the management of type 2 diabetes, and provides suggestions for the potential relevance of these agents in the management of dysglycaemia in the critically ill, particularly to normalise elevated blood glucose levels.
Highlights
Hyperglycaemia occurs frequently in the critically ill, even in those patients without a history of diabetes
Hyperglycaemia occurs frequently in patients without known diabetes; this group includes patients with undiagnosed type 2 diabetes and those with so-called stress hyperglycaemia. We propose that the latter should be referred to as critical illness induced hyperglycaemia (CIIH), given that this describes the pathogenesis more appropriately
CIIH is characterised by hyperglycaemia in critically ill patients, who were glucose tolerant prior to their acute illness, and are shown in the longer term not to have diabetes [1]
Summary
The discovery of the incretin hormones has encouraged a burgeoning pharmaceutical industry that exploits the entero-insular axis. As the prevalence of T2DM and the use of incretin-based regimens continue to rise, the intensivist is likely to encounter more patients who were taking these drugs prior to their acute illness. The pharmacologic strategy of administering incretin mimetics to manage acute hyperglycaemia in the critically ill, while minimising the risk of hypoglycaemia and mitigating glycaemic variability, is appealing. Future studies should focus on the identification of the patient groups most likely to benefit from the administration of incretin receptor agonists, which of the agents is most useful in the critically ill, and at what dose, the relevance of the route of feeding with concurrent incretin therapy and, whether these agents should be used in combination with insulin or as singleagent therapy to provide a safer, more effective and simpler method of achieving glycaemic control. The remaining authors declare that they have no competing interests
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