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Potassium In Dka

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Determinants Of Plasma Potassium Levels In Diabetic Ketoacidosis.

1. Medicine (Baltimore). 1986 May;65(3):163-72. Determinants of plasma potassium levels in diabetic ketoacidosis. Adrogu HJ, Lederer ED, Suki WN, Eknoyan G. The classic proposal of intracellular K+ for extracellular H+ exchange asresponsible for the hyperkalemia of diabetic ketoacidosis (DKA) has beenquestioned because experimentally induced organic anion acidosis fails to producehyperkalemia. It has been suggested, instead, that the elevated serum [K+] of DKAmight be the result of the compromised renal function, secondary to volumedepletion, that usually accompanies DKA. However, several metabolic derangements other than volume depletion and acidosis, which are known to alter potassiummetabolism, also develop in DKA. This study of 142 admissions for DKA examinesthe possible role of alterations in plasma pH, bicarbonate, glucose (G),osmolality, blood urea nitrogen (BUN) and plasma anion gap (AG) on the levels of [K+]p on admission. Significant (p less than 0.01) correlations of [K+]p witheach of these parameters were found that could individually account for 8 to 15percent of the observed variance in the plasma potassium levels; however, theeffects of some or all of these paramete Continue reading >>

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  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

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Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 a Continue reading >>

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  1. nurseprnRN

    The hypokalemia comes when the patient gets treated with insulin, driving the glucose and K+ into the cells. The kidneys can't (and won't) move so much out through urine with the excess glucose to make for hypokalemia.

  2. Esme12

    There can be a brief period of hypoglycemia in the early stages of an elevated blood sugar (polyuria)....but by the time "ketoacidosis" sets in the Serum potassium is elevated but the cellular potassium is depleted (all that shifting that goes on)
    Diabetic ketoacidosis

  3. April2152

    So pretty much what we would observe clinically is hyperkalemia because the osmotic duiresis does not move serum potassium significantly?

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Hyperkalaemia In Diabetic Ketoacidosis

Dear Editor, I have a brief comment on the informative ‘Lesson of the week’ by Moulik and colleagues, describing an association between hyperkalaemia and an ECG pattern suggesting acute myocardial infarction in a patient with diabetic ketoacidosis (DKA). One of the mechanisms of hyperkalaemia in DKA stated at the beginning of the Discussion is not strictly correct. It is inorganic acids, and not organic acids (including lactic acid), that cause hyperkalaemia as a result of potassium ions leaving cells in ‘exchange’ for hydrogen ion entry (and their intracellular buffering). In DKA, the key mechanism is lack of insulin, which is probably the most important short-term regulator of plasma potassium concentration (through stimulation of the cell ‘sodium’ pump – Na,K-ATPase) and defence against acute hyperkalaemia resulting from our daily intake of potassium (~80 mmol): The extracellular pool of potassium is around 65 mmol and could almost double after a single steak meal (~50 mmol), which is too rapid a change for compensatory renal excretion. In DKA, an additional mechanism is the osmotic shrinkage of cells as a result of the high plasma glucose concentration (and plasma Continue reading >>

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Popular Questions

  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

  4. -> Continue reading
read more

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