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Diabetic Ketoacidosis with Case

by Michael Lazarus, MD

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      Slides 02-03 Diabetes Melitus part 2.pdf
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    00:00 The acute complications of diabetes mellitus include diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Acute complications of uncontrolled hyperglycemia with life-threatening consequences can occur if not recognized and treated early. Let's go to this case. A 10-year-old boy is brought to the emergency department by his mother due to frequent vomiting, abdominal pain, and weakness. Over the last 5 days, he felt excessively thirsty and has been urinating frequently.

    00:33 Family history is non-contributory. His temperature is 37.1°C, his blood pressure is 100/70, and his pulse rate 110 beats/minute. On physical exam, he is non-responsive to verbal commands.

    00:47 He has sunken eyes, poor skin turgor, and rapid deep respirations. His lab findings reveal a random plasma glucose of 460 mg/dL. He has an undetectable fasting C-peptide, his serum beta-hydroxybutyrate is elevated, and his GAD antibodies are positive. What is the most likely diagnosis? This is a young boy with vomiting, abdominal pain, and weakness that is progressive. He also manifested with polydipsia and polyuria. Signs of dehydration and tachypnea, that is shallow and rapid respiration, are also present which makes us suspect a respiratory alkalosis. He also has profound hypoglycemia. The presence of undetectable fasting C-peptide is an indication that he has no endogenous insulin production. Also, the fact that his serum ketones are elevated confirms the presence of diabetic ketoacidosis. And finally, the positive GAD antibodies imply that the etiology of his type 1 diabetes is an immune-mediated process. And confirming the diagnosis, this young boy has presented in acute diabetic ketoacidosis. DKA typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency and an increase in counter-regulatory hormones.

    02:18 Sufficient amount of insulin are not present to suppress lipolysis and oxidation of free fatty acids. This in turn leads to ketone body production by the body and a subsequent metabolic acidosis.

    02:32 DKA occurs more frequently with type 1 diabetes, although 10-30% of it can occur in patients with type 2 diabetes. It may be the initial clinical presentation in some patients with previously undiagnosed type 1 or type 2 diabetes.


    About the Lecture

    The lecture Diabetic Ketoacidosis with Case by Michael Lazarus, MD is from the course Diabetes Mellitus. It contains the following chapters:

    • Complications of Type 2 DM
    • Case: 10-year-old Boy with Vomiting and Abdominal Pain
    • Diabetic Ketoacidosis

    Included Quiz Questions

    1. Diabetic ketoacidosis
    2. Myxedema coma
    3. Hyperosmolar hyperglycemic state
    4. Type 1 diabetes mellitus
    1. Decreased endogenous insulin production, suggesting type 1 diabetes
    2. In conjunction with an elevated plasma glucose level, it suggests the surreptitious injection of a family member's insulin
    3. Increased endogenous insulin production, suggesting type 2 diabetes
    4. A high level of insulin resistance, suggesting type 2 diabetes
    5. Production of insulin from somewhere other than the pancreas, such as an insulin-producing neuroendocrine tumor
    1. Low insulin levels cause the body to obtain energy through the oxidation of free fatty acids, of which ketone bodies are a byproduct.
    2. A large gap metabolic acidosis induces the release of ketone bodies.
    3. Insulin resistance directly causes the pancreas to produce ketones.
    4. Ketoacidosis occurs randomly in patients with type 1 and type 2 diabetes.
    5. High levels of insulin stimulate the breakdown of fats, which in turn causes the release of ketones.

    Author of lecture Diabetic Ketoacidosis with Case

     Michael Lazarus, MD

    Michael Lazarus, MD


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