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Hyperglycemic Crises in Diabetes

Abbreviations: ß-OHB, ß-hydroxybutyric acid • AKA, alcoholic ketoacidosis • DKA, diabetic ketoacidosis • HHS, hyperosmolar hyperglycemic state

The first 300 words of the full text of this article appear below.

	INTRODUCTION

 
Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at 15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10).

This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information.

	PATHOGENESIS

 
Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (ß-hydroxybutyrate [ß-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are inadequate to facilitate glucose utilization by insulin-sensitive tissues but adequate (as determined by residual C-peptide) to prevent lipolysis and subsequent ketogenesis, although the evidence for this is weak (14. . . [Full Text of this Article]

	PRECIPITATING FACTORS

 

	DIAGNOSIS

 
History and physical examination
Laboratory findings
Differential diagnosis

	TREATMENT

 
Fluid therapy
Adult patients.
Pediatric patients (<20 years of age).
Insulin therapy
Potassium
Bicarbonate
Phosphate

	COMPLICATIONS

 

	PREVENTION

 

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Related Article:

POSITION STATEMENTS & ADA STATEMENTS
Diabetes Care 2006 29: S75-S77. [Extract] [Full Text] [PDF]