Stress induced hyperglycaemia (S.I.H) is common in critically ill patients.
a) Define S.I.H
b) Outline the mechanisms thought important in the pathogenesis of S.I.H.
c) Outline clinical implications and treatment of S.I.H.
a) Define S.I.H
Transient hyperglycaemia during acute illness –usually restricted to patients without prior evidence of diabetes with reversion to normal after discharge.
b) Outline the mechanisms thought important in the pathogenesis of S.I.H.
• S.I.H is thought to develop due to complex interplay between counter regulatory hormones such as catecholamines, GH, cortisol and cytokines.
• The underlying illness and treatments (TPN, enteral feed, steroids, and vasopressors) might affect the scale of these derangements.
• The key contributor would appear to be high hepatic glucose output via gluconeogenesis driven by glucagon, adrenaline and cortisol. Cytokines such as TNFα interact to enhance this response.
• Insulin resistance plays a role.
• Underlying abnormalities in glucose regulation may be present.
c) Outline clinical implications and treatment of S.I.H.
• Recent data suggests that S.I.H and diabetic hyperglycaemia are two different phenomena with differing clinical outcomes.
• Patients with S.I.H have been shown in several studies to have increased risk of mortality, adverse events, and greater organ failure scores compared to those with diabetes.
• Whether S.I.H per se causes harm or instead is a marker of severity of counter regulatory response and degree of illness is unknown.
• Management of S.I.H cannot be distinguished from hyperglycaemia due to other causes. In most cases it is not generally predictable or preventable. Early recognition and interception might prevent persistence and exacerbation. Recommendations include insulin therapy with more conservative glucose targets.
• Candidates mentioning recent data from RCTs were given credit.
Stress-induced hyperglycaemia is discussed elsewhere. In brief, one would define it as hyperglycaemis which occurs in the presence of severe illness and in the absence of pre-existing diabetes. Marik & Bellomo have a nice review of this from 2013.
One could summarise the mechanisms as follows:
Clinical implications of stress-induced hyperglycaemia and its treatment are detailed in the chapter on glycaemic conrol in critical illness.
The key points can be summarised as a list:
The college points out that association with mortality is not evidence of causation. Glucose may just be another acute phase reactant.
And as for management? In short, keep the BSL between 5 and 8. Finfer et al have demonstrated (NICE-SUGAR) that tight glycaemic control hurts more people than it helps.
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.
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.