Tutorial 6 Ketoacidosis

This tutorial looks at the problem of ketoacidosis and, in particular, focuses on diabetic ketoacidosis. Ketones are produced from free fatty acids in the liver, converted to acetyl coenzyme A and oxidatively metabolized for energy production or packaged in the form of acetoacetate or beta hydroxybutyrate and exported to the tissues. This occurs continuously in the body. Control over metabolism is provided by insulin. When insulin levels are high glucose is utilized primarily for energy production and fatty acid metabolism is curtailed. When insulin levels are low fatty acids become the primary source of energy. In situations of very low carbohydrate intake ketones may be measurable in the blood and we call this ketosis. When plasma ketones exceed 3 millimoles per liter this results in a strong ion effect and ketoacidosis. This is generally only seen in states of metabolic failure such as type 1diabetes starvation and alcoholism.
The ketones acetoacetate and beta hydroxybutyrate are strong anions and cause metabolic acidosis when they accumulate. This manifests as a fall in the bicarbonate and an increase in the base deficit. Classically there is a widened anion gap metabolic acidosis with full respiratory compensation. Nevertheless the extent of the acidosis is rarely explained by ketones alone. Lactic acidosis is frequently present as is acidosis caused by the accumulation of metabolic junk products. Iatrogenic metabolic acidosis may ensue caused by the administration of hyperchloremic (0.9% NaCl + KCl) saline solutions.
Diabetic ketoacidosis is characterized by loss of control of blood glucose, loss of control of blood lipids and hypercatabolism of proteins. Failure to suppress gluconeogenesis within the liver depletes the tricarboxylic acid cycle reserves and results in uncontrolled ketone production. Patients become hyperglycemic glycosuric, keto acidotic, initially hyponatremic, later hypernatremic, and hyperkalemic. The treatment is to fluid resuscitate the patient, administer insulin by intravenous infusion, replenish glycogen stores and provide glucose for intracellular substrate and prevent further ketone production. Extra care must be taken to avoid hypoglycemia and hypokalemia.
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Description
00:40 Introduction
01:53 Clinical Scenarios (Laura and Declan)
04:20 Basic Metabolism
05:40 Insulin Is the Monarch of Metabolism
07:30 What Happens To Metabolism in Starvation (auto-cannibalism)
08:25 Ketone Production
10:20 Metabolic Failure
11:00 Ketosis vs Ketoacidosis
14:50 Diabetic Ketoacidosis - definition
16:40 Diabetic Ketoacidosis - components
19:00 Measuring Ketones
21:00 The Acidosis in DKA (it’s not only ketones, not even close)
22:25 Dysnatremias in DKA (hyponatremia, hypernatremia)
24:30 Management of DKA (and overview not a prescriptive “protocol”)
28:48 Controversies and Concerns in Management of DKA
30:54 Insulin Infusions
31:42 Clinical Scenarios (Laura and Declan) Resolved
33:50 Review and Preview