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:

  • Question 4 from the first paper of 2010 (stress-induced hyperglycaemia)
  • Question 24 from the first paper of 2006 (causes of hyperglycaemia)
  • Question 7 from the first paper of 2002 (causes of hyperglycaemia)

If one were to recommend any single resource for the panicked last-minute revision of this topic, it would be Marik & Bellomo (2013)

Definition of stress-induced hyperglycaemia

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:

  • Hyperglycaemia which is
    • Transient
    • Reversible
    • Associated with severe acute illness
    • In a patient previously not diabetic

Pathogenesis of stress-induced hyperglycaemia

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.

stress induced hyperglycaemia

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:

  • Increased glucose synthesis is due to the following mechanisms:
    • Increased lipolysis due to catecholamine activity
    • Increased gluconeogenesis due to catecholamine activity
    • Increased glycogenolysis due to catecholamine activity
  • Increased insulin resistance is due to the decreased sensitivity of skeletal muscle to insulin, via the effects of the following hormones:
    • Catecholamines
    • Growth hormone
    • Cortisol
    • TNF-α
  • Additional effects are the direct inhibition of insulin release by adrenaline, and the activation of hepatic glycolysis by glucagon.

Causes of hyperglycaemia in the ICU

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.

Causes of Hyperglycaemia in the ICU

Insulin resistance

  • NIDDM
  • Stress response
  • Corticosteroid therapy
  • Cushings disease

Inadequate insulin levels

  • Under-supplemented
  • Stress response
  • Pancreatitis
  • Haemochromatosis
  • Insulin antibodies

Excessive endogenous glucose release

  • Catecholamine infusion
  • Stress response
  • Glucagon administration

Excessive exogenous glucose supplements

  • TPN with 50% dextrose
  • Inappropriately sugary IV fluids
  • Overfeeding with enteric nutrition
  • Glucose-containing peritoneal dialysis fluid

Consequences of hyperglycaemia are well discussed in the natural follow-on from this chapter, the discussion of glycaemic control in critical illness.

References

McCowen, Karen C., Atul Malhotra, and Bruce R. Bistrian. "Stress-induced hyperglycemia." Critical care clinics 17.1 (2001): 107-124.

Falciglia, Mercedes, et al. "Hyperglycemia-related mortality in critically ill patients varies with admission diagnosis." Critical care medicine 37.12 (2009): 3001.

Falciglia, Mercedes. "Causes and consequences of hyperglycemia in critical illness." Current Opinion in Clinical Nutrition & Metabolic Care 10.4 (2007): 498-503.

Finfer, Simon, et al. "Intensive versus conventional glucose control in critically ill patients." N Engl J Med 360.13 (2009): 1283-1297.

Marik, Paul E., and Rinaldo Bellomo. "Stress hyperglycemia: an essential survival response!." Critical Care 17.2 (2013): 305.