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Hyperglycaemia and mortality from acute stroke

F Tracey1, V L Crawford, J T Lawson

  • 1Department of Geriatric Medicine, Queen's University of Belfast.

The Quarterly Journal of Medicine
|July 1, 1993
PubMed
Summary
This summary is machine-generated.

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Hyperglycaemia after acute stroke is linked to stress, not direct harm to brain tissue. This finding suggests current treatments for high blood sugar in stroke patients may need re-evaluation.

Area of Science:

  • Neurology
  • Endocrinology
  • Medical Research

Background:

  • Hyperglycaemia is frequently observed in acute stroke patients.
  • A poor prognosis is associated with elevated glucose levels post-stroke.
  • The cause of hyperglycaemia (stress response vs. direct tissue damage) remains unclear.

Purpose of the Study:

  • To investigate the relationship between acute stroke, hyperglycaemia, and patient outcomes.
  • To determine if hyperglycaemia is a direct cause of neurological damage or a result of the stress response.
  • To explore the role of stress hormones and HbA1c in acute stroke patients without diabetes.

Main Methods:

  • Seventy-one non-diabetic acute stroke patients were recruited.
  • Fasting blood samples were collected within 24 hours for glucose, stress hormones (cortisol), and HbA1c.

Related Experiment Videos

  • Brain CT scans and 3-month follow-up for mortality were conducted.

    • Main Results:

    • Higher glucose levels correlated with mortality, but this was not significant after accounting for age and cortisol levels.
    • Serum cortisol levels showed a stronger correlation with lesion volume than glucose levels.
    • Haemoglobin A1c showed no association with mortality or lesion volume.

    Conclusions:

    • The hyperglycaemia observed in acute stroke appears to be a secondary stress response.
    • Evidence does not support the hypothesis that hyperglycaemia directly harms ischaemic brain tissue.
    • Findings have implications for the use of hypoglycaemic agents in acute stroke management.