Diabetes Mellitus Acute Complications

Overview
  • Acute complications of Type I or Type II Diabetes Mellitus (DM) can arise over hours to days in individuals and result from absolute or relative insufficiency of insulin. Acute complications are highly serious and in the absence of treatment can rapidly result in death. The basic etiology of these acute complications is an inability to properly metabolize glucose, resulting in hyperglycemia. However, disease tends to manifest along a spectrum with the ends being termed "Diabetic Ketoacidosis" (DKA) and "Hyperglycemic Hyperosmolar State" (HHS), discussed separately below.
Diabetic Ketoacidosis
  • Pathogenesis
    • Diabetic Ketoacidosis (DKA) is typically associated with Type I DM although it can occur in some patients with Type II DM as well. The pathogenesis of DKA requires both an absolute insufficiency of insulin along with excess of other hormones which boost blood glucose concentration such as glucagon, cortisol, circulating catecholamines, or growth hormone. This endocrine environment results in an inability of the body's tissues to import and metabolize glucose, resulting in hyperglycemia. In addition, alterations in adipose tissue metabolism result in adipocytes metabolizing and exporting fatty acids which upon reaching the metabolically-altered liver are converted into ketoacids. Therefore, DKA results in both hyperglycemia and ketosis.
  • Clinical Consequences
    • Hyperglycemia associated with DKA results in polyuria and ultimately volume depletion which may lead to hypotension and associated tachycardia. Release of large amounts of ketoacids give the patient's breath a characteristic fruity odor and can affect acid-base homeostasis, resulting in metabolic acidosis. Intense abdominal pain, nausea, and vomiting are also associated with DKA. If not treated promptly, patients with DKA can progress to coma within hours todays.
Hyperglycemic Hyperosmolar State
  • Pathogenesis
    • Hyperglycemic Hyperosmolar State (HHS) is typically associated with Type II DM and results from a relative insufficiency of insulin that cannot overcome the insulin resistance that occurs in patients with Type II DM. Patients who develop HHS retain some capacity to synthesize and respond to Insulin, resulting in a milder clinical syndrome that DKA. Consequently, hyperglycemia occurs in the absence of ketosis although it is poorly understood why this is the case.
  • Clinical Consequences
    • The hyperglycemia of HHS results in polyuria which leads to volume depletion and ultimately hypotension associated with tachycardia. Happily, signs and symptoms of ketosis are not observed although there are mild elevations of ketoacids in those with HHS.