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Why Is Potassium Given In Diabetic Ketoacidosis?

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Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, co Continue reading >>

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  1. * DKA explanation

    * DKA explanation

    Below you will find a terrific explanation of DKA from one of the instructors at Med School Tutors. If you like what you see and may be interested in learning more about one-on-one instruction from MST, then please visit their website at www.medschooltutors.com
    In order to understand how to treat DKA, it is useful to first understand what is going on in the body when DKA develops. First of all, DKA (diabetic ketoacidosis) typically develops when a Type I diabetic does not take his or her insulin for a prolonged period of time. It may also be the presentation for new onset diabetes. Because these patients are insulin deficient, they are not able to take up glucose into their cells. This results in two important consequences: 1)glucose builds up in the blood and causes hyperglycemia and 2)the body's cells are forced to breakdown fat for energy, instead of glucose.
    These are very significant consequences... The hyperglycemia results in an osmotic diuresis, because the proximal tubule of the kidney can't reabsorb all the glucose filtered into the nephron. What is osmotic diuresis? Simply that the hyperglycemia (usually >300) causes the body to excrete lots and lots of water, because the osmotic pull of all the glucose particles prevents the reabsorbtion of water in the collecting duct. This means that patients with DKA are peeing their brains out!! They pee out sodium, potassium, and water.. And are therefore, very very very DEHYDRATED, sodium depleted, and potassium depleted.
    Now for the metabolism end of things... The body cells are forced to metabolize fat for energy rather than glucose. How do they accomplish this? - beta-oxidation of fatty acids. This results in excess production of ketone bodies which deplete available acid buffers. This causes a significant metabolic acidosis, with a high anion gap due to the presence of ketoacids. The acidosis causes potassium to shift from the intracellular space to the extracellular space. This may result in a normal or high serum potassium level. This normal or high potassium level masks what is typically significant potassium depletion because the person was peeing all their potassium out as a result of the uncontrolled hyperglycemia.
    So what are we going to do now? I will give a very brief answer for now, expect people to ask questions in the meantime, and then provide a more thorough approach to treatment in the coming days.
    1)Give the patient tons of normal saline. Why? - because your patient is dehydrated as all hell. They have been peeing out every last drop of water because of their severe uncontrolled hyperglycemia. These patients require liters of fluid to replenish all the fluid they've lost as a result of the osmotic diuresis.
    2)Give them insulin. Why? - NOT because it will lower the blood glucose level, but because it will cause a shift away from fat metabolism and toward glucose metabolism. This will slow the production of ketone bodies which are precipitating the metabolic acidosis. Thus, I will repeat, we give insulin to shift away from fat metabolism and stop the production of ketone bodies.
    3)Give the patient potassium. Why? - As we discussed earlier, the person has been peeing out all of their potassium stores and are overall very potassium depleted, despite having normal or high serum potassium levels to begin with. In addition to being potassium depleted, the insulin you are giving will cause a shift of potassium from the extracellular space to the intracellular space, which will drop the serum potassium. Thus, we give DKA patients potassium way before they become hypokalemic.
    4)Give the patient dextrose. Why? - They insulin you are giving the patient is obviously going to cause the serum glucose to decrease. We give glucose to prevent hypoglycemia as we continue to give insulin.
    How do we know when we are finished treating these patients? - When the anion gap returns to normal.
    That's all for now. Please ask any questions you have. I will be giving more specifics about DKA management in the near future.
    PS: Does anyone know the dangerous consequence of giving DKA patients fluid too rapidly? What are the symptoms this may cause, and what is the pathophysiology behind these symptoms?

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