CICM SAQ 2010.1 Q4

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.