This is a disorder of glucose metabolism, due to increased gluconeogenesis and glycogenolysis, which occurs as a result of cortisol and catecholamine excess in critical illness. It is a part of the stereotypical "stress response" to physiological adversity. CICM SAQs about stress-induced hypoglycaemia have included the following:
If one were to recommend any single resource for the panicked last-minute revision of this topic, it would be Marik & Bellomo (2013).
The college answer to Question 4 from the first paper of 2010 reports that SIH is defined as "transient hyperglycaemia during acute illness –usually restricted to patients without prior evidence of diabetes with reversion to normal after discharge." Indeed, the basic definition is:
Not all problems in education can be solved with a flowchart, particularly in the case of metabolic biochemistry and physiology. Having said that, here is a flowchart.
Hyperglycaemia results from both a stress-induced release of glucose, and a stress-hormone-induced resistance to insulin (LITFL tells me that this is the most important component).
For the purposes of revision, one could summarise the mechanisms as follows:
Rather than label every hyperglycaemic ICU patient as a sufferer of stress-induced hyperglycaemia, it is important to recognise that there are a massive variety of various random causes of hyperglycaemia in critical illness.
Inadequate insulin levels
Excessive endogenous glucose release
Excessive exogenous glucose supplements
Consequences of hyperglycaemia are well discussed in the natural follow-on from this chapter, the discussion of glycaemic control in critical illness.