John has Type 1 Diabetes. He has a stomach virus and cannot keep any food down.

Question

John has Type 1 Diabetes. He has a stomach virus and cannot keep any food down. He feels sluggish and cannot think straight.   He has vomited 3 times in an hour. As a result, his body has gone into ketoacidosis.   A. Explain to me how his body has reached this state metabolically (what is happening on a cellular/molecular level) Hint: Think about the absorptive vs post absorptive state to remember what our body does with key nutrients. Remember glucose is our favorite!!   B. What form of acidosis does John have and how do you know? C. How would clinicians treat John and why is this best way to treat his imbalance

Explanation / Answer

A. Insulin deficiency causes the body to metabolize triglycerides and amino acids instead of glucose for energy. Serum levels of glycerol and free fatty acids (FFAs) rise because of unrestrained lipolysis, due to muscle catabolism. Glycerol and alanine provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of glucagon that accompanies insulin deficiency.

Glucagon also stimulates mitochondrial conversion of FFAs into ketones. Insulin normally blocks ketogenesis by inhibiting the transport of FFA derivatives into the mitochondrial matrix, but ketogenesis proceeds in the absence of insulin. The major ketoacids produced were acetoacetic acid and beta-hydroxybutyric acid which are the strong organic acids that create metabolic acidosis. Acetone derived from the metabolism of acetoacetic acid accumulates in serum and is slowly disposed of by respiration.

Hyperglycemia due to insulin deficiency causes an osmotic diuresis that leads to marked urinary losses of water and electrolytes. Urinary excretion of ketones obligates additional losses of sodium and potassium. Serum sodium may fall due to natriuresis or rise due to excretion of large volumes of free water. Potassium is also lost in large quantities. Despite a significant total body deficit of potassium, initial serum potassium is typically normal or elevated because of the extracellular migration of potassium in response to acidosis. Potassium levels generally fall further during treatment as insulin therapy drives potassium into cells. If serum potassium is not monitored and replaced as needed, life-threatening hypokalemia may occur.

B. John is having Ketoacidosis. This can be confirmed by symptoms like nausea, vomiting and abdominal pain. Additionally, we can diagnose this by symptoms like excessive thirst, frequent urination, shortness of breath, fruity-scented breath and confusion. Other laboratory abnormalities include hyponatremia, elevated serum creatinine, and elevated plasma osmolality.

C. Clinically the treatment was done by volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia. Volume repletion can be done by IV fluid 0.9% saline. Hyperglycemia is corrected by giving regular insulin 0.1 unit/kg IV bolus initially, followed by continuous IV infusion of 0.1 unit/kg/h in 0.9% saline solution. Ketones should begin to clear within hours if insulin is given in sufficient doses. Hypokalemia prevention requires replacement of 20 to 30 mEq potassium in each liter of IV fluid to keep serum potassium in a moderate range.

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