Tag Archives: Hypokalemia

Potassium abnormalities in a pediatric intensive care unit: frequency and severity. (Williams)

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Cummings BM, Macklin EA, Yager PH, Sharma A, Noviski N. Potassium abnormalities in a pediatric intensive care unit: frequency and severity. J Intensive Care Med. 2014 Sep;29(5):269-74.

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BACKGROUND: Potassium abnormalities are common in critically ill patients. We describe the spectrum of potassium abnormalities in our tertiary-level pediatric intensive care unit (PICU).

METHODS: Retrospective observational cohort of all the patients admitted to a single-center tertiary PICU over a 1-year period. Medical records and laboratory results were obtained through a central electronic data repository.

RESULTS: A total of 512 patients had a potassium measurement. Of a total of 4484 potassium measurements, one-third had abnormal values. Hypokalemia affected 40% of the admissions. Mild hypokalemia (3-3.4 mmol/L) affected 24% of the admissions. Moderate or severe hypokalemia (K < 3.0 mmol/L) affected 16% of the admissions. Hyperkalemia affected 29% of the admissions. Mild hyperkalemia (5.1-6.0 mmol/L) affected 17% of the admissions. Moderate or severe hyperkalemia (>6.0 mmol/L) affected 12%. Hemolysis affected 2% of all the samples and 24% of hyperkalemic values. On univariate analysis, severity of hypokalemia was associated with mortality (odds ratio 2.2, P = .003).

CONCLUSIONS: Mild potassium abnormalities are common in the PICU. Repeating hemolyzed hyperkalemic samples may be beneficial. Guidance in monitoring frequencies of potassium abnormalities in pediatric critical care is needed.

Hypokalemia during treatment of diabetic ketoacidosis: clinical evidence for an aldosterone-like action of insulin. (Hebbar)

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J Pediatr. 2013 Jul;163(1):207-212.e1. PMID: 23410602

OBJECTIVES: To investigate whether the development of hypokalemia in patients with diabetic ketoacidosis (DKA) treated in the pediatric critical care unit (PCCU) could be caused by increased potassium (K(+)) excretion and its association with insulin treatment.

STUDY DESIGN: In this prospective observational study of patients with DKA admitted to the PCCU, blood and timed urine samples were collected for measurement of sodium (Na(+)), K(+), and creatinine concentrations and for calculations of Na(+) and K(+) balances. K(+) excretion rate was expressed as urine K(+)-to-creatinine ratio and fractional excretion of K(+).

RESULTS: Of 31 patients, 25 (81%) developed hypokalemia (plasma K(+) concentration <3.5 mmol/L) in the PCCU at a median time of 24 hours after therapy began. At nadir plasma K(+) concentration, urine K(+)-to-creatinine ratio and fractional excretion of K(+) were greater in patients who developed hypokalemia compared with those without hypokalemia (19.8 vs 6.7, P = .04; and 31.3% vs 9.4%, P = .004, respectively). Patients in the hypokalemia group received a continuous infusion of intravenous insulin for a longer time (36.5 vs 20 hours, P = .015) and greater amount of Na(+) (19.4 vs 12.8 mmol/kg, P = .02). At peak kaliuresis, insulin dose was higher in the hypokalemia group (median 0.07, range 0-0.24 vs median 0.025, range 0-0.05 IU/kg; P = .01), and there was a significant correlation between K(+) and Na(+) excretion (r = 0.67, P < .0001).

CONCLUSIONS: Hypokalemia was a delayed complication of DKA treatment in the PCCU, associated with high K(+) and Na(+) excretion rates and a prolonged infusion of high doses of insulin.

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