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Hyperglycemia crisis and hypoglycemia are both life-threatening medical emergencies but are usually readily treatable if recognized early. Hyperglycemic crises comprise diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). While some elements of their clinical presentation and pathophysiology are distinct, the general principles of treatment are similar. They will be discussed together. Hypoglycemia is a problem commonly seen in patients with diabetes mellitus (DM) and requires prompt treatment. The common causes and treatment regimens will be outlined here.



  • Hyperglycemic crisis has a high mortality, particularly in the elderly.

  • Mortality rates are falling due to improved recognition and medical care.

  • Fluid volume restoration, insulin, and electrolyte management are key.

  • Regular electrolyte and glycemic assessment is needed.

  • DKA is more commonly seen in younger patients with type 1 DM.

  • Patients presenting with HHS are often older with type 2 DM.

  • Precipitating causes should be sought.


Serum glucose is a continuum and there is a spectrum of hyperglycemia. DKA and HHS represent the extremes of hyperglycemia and are regarded as medical emergencies. Hyperglycemia is caused by a relative insulin insufficiency. This may be caused by any combination of

  • a) Decreased insulin production

  • b) Increased insulin requirements

  • c) Increased counterregulatory hormones

  • d) Decreased peripheral glucose utilization

In type 1 diabetes mellitus (DM), autoimmune-mediated β-cell death leads to a dramatic fall, and eventually a complete cessation, of insulin production. This can lead to hyperglycemia over a very short period of time. In type 2 DM, there is lowered insulin sensitivity, increased hepatic gluconeogenesis, and a more gradual reduction in insulin secretion over years. Traditionally DKA was seen almost exclusively in patients with type 1 DM, while HHS was a rare complication of elderly patients with type 2 DM. HHS has supplanted the older terms hyperglycemic hyperosmolar nonketotic coma and hyperglycemic hyperosmolar nonketotic state. This change reflects that patients with HHS may have detectable ketonemia and need not have an altered sensorium or present with coma.

Profound insulin deficiency leads to conversion of excess fatty acid to acetyl coenzyme A (ACA) via β-oxidation. Ordinarily ACA would be further oxidized via the TCA cycle. In the absence of insulin, excess amounts of ACA form ketone bodies (acetone, acetoacetate, and B-hydroxybutyrate) via acetoacyl-CoA and β-hydroxy-β-methylglutaryl-CoA. Ketone bodies are produced in small physiologically acceptable amounts (<0.5 mM) in the fasting state when carbohydrate is unavailable or inaccessible for short periods of time. However, hyperketonemia (>1 mM, usually >3.0 mM in ketoacidosis) can result in a raised anion gap metabolic acidosis, ketonuria, dehydration, and electrolyte imbalance.1

Ketonemia and ketoacidosis are classically seen in patients with type 1 DM leading to DKA. However, DKA can be seen in any form of DM with significant insulin deficiency, usually during times of physiological stress (eg, sepsis, cardiovascular event, or trauma). ...

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