Incidence of hypoglycemia following insulin‐based acute stabilization of hyperkalemia treatment

Schafers, Stephen J.; Naunheim, Rosanne; Vijayan, Anitha; Tobin, Garry S.

doi:10.1002/jhm.977

Cited by 61 publications

(92 citation statements)

References 14 publications

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“…The proximate causes of hypoglycemia in our study population included excessive insulin doses, inadequate monitoring of blood glucose trends, changes in nutritional status without a change in the antidiabetic therapy, nursing administration errors, and insufficient glucose with insulin for acute treatment of hyperkalemia. Consequently, interventions were developed that included: a recommended change in the treatment for acute hyperkalemia, 25 creation of a nursing educational tool that focuses on using critical thinking skills in the assessment of patients receiving insulin, implementation of a case-based insulin dosing curriculum for all medical staff, and a redesign of the hospital's supplementary insulin dosing protocols for bedtime administration. These changes have decreased the rate of SH <40 mg/dl from a rate of 5.01 events per 1000 at-risk patient days in 2008 to 3.90 per 1000 at-risk patient days in 2010 at Barnes-Jewish Hospital.…”

Section: The Diabetes Control and Complications Trial Reportedmentioning

confidence: 99%

Prediction and Prevention of Treatment-Related Inpatient Hypoglycemia

Elliott

Schafers

McGill

et al. 2012

J Diabetes Sci Technol

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Section: The Diabetes Control and Complications Trial Reportedmentioning

confidence: 99%

Prediction and Prevention of Treatment-Related Inpatient Hypoglycemia

Elliott

Schafers

McGill

et al. 2012

J Diabetes Sci Technol

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“…There appear to be fewer hypoglycemic events when the glucose dose is larger, when the insulin bolus is given after the glucose infusion rather than before it and when the treatment is given as a constant infusion over 60 min rather than as a bolus. Careful clinical monitoring and repeated measurements of blood glucose are recommended for several hours after insulin therapy [17,18]. …”

Section: Discussionmentioning

confidence: 99%

“…In this way, insulin therapy rapidly and reliably lowers serum [K + ], but this comes at the cost of frequent episodes of hypoglycemia, even when glucose is given concurrently to try and prevent this complication [13,14,15,16]. Hypoglycemia is a serious and common adverse effect of insulin therapy and may manifest several hours after insulin administration [17,18]. …”

Section: Introductionmentioning

confidence: 99%

Bolus Administration of Intravenous Glucose in the Treatment of Hyperkalemia: A Randomized Controlled Trial

et al. 2014

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Background: Hyperkalemia is a common medical emergency that may result in serious cardiac arrhythmias. Standard therapy with insulin plus glucose reliably lowers the serum potassium concentration ([K⁺]) but carries the risk of hypoglycemia. This study examined whether an intravenous glucose-only bolus lowers serum [K⁺] in stable, nondiabetic, hyperkalemic patients and compared this intervention with insulin-plus-glucose therapy. Methods: A randomized, crossover study was conducted in 10 chronic hemodialysis patients who were prone to hyperkalemia. Administration of 10 units of insulin with 100 ml of 50% glucose (50 g) was compared with the administration of 100 ml of 50% glucose only. Serum [K⁺] was measured up to 60 min. Patients were monitored for hypoglycemia and EKG changes. Results: Baseline serum [K⁺] was 6.01 ± 0.87 and 6.23 ± 1.20 mmol/l in the insulin and glucose-only groups, respectively (p = 0.45). At 60 min, the glucose-only group had a fall in [K⁺] of 0.50 ± 0.31 mmol/l (p < 0.001). In the insulin group, there was a fall of 0.83 ± 0.53 mmol/l at 60 min (p < 0.001) and a lower serum [K⁺] at that time compared to the glucose-only group (5.18 ± 0.76 vs. 5.73 ± 1.12 mmol/l, respectively; p = 0.01). In the glucose-only group, the glucose area under the curve (AUC) was greater and the insulin AUC was smaller. Two patients in the insulin group developed hypoglycemia. Conclusion: Infusion of a glucose-only bolus caused a clinically significant decrease in serum [K⁺] without any episodes of hypoglycemia.

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“…hydrophobic interaction. Different modifications in the structure of insulin have been made to affect insulin [9][10][11][12][13][14][15][16][17][18][19][20][21]. Insulin has the tendency to undergo for the structural transformation and results in aggregation and formation of insoluble insulin fibrils.…”

Section: Introductionmentioning

confidence: 99%

“…The absolute mechanism of the formation of the fibril is still unclear. Therefore, most popular methods for the stabilization of the insulin against fibrillation contribute to counteract associated insulin from being disassembled [2, [9][10][11][12][13]22]. It is evident that the stabilization mechanism is consistent with the destabilising role attributed to hydrophobic surfaces [14][15][16][17][18][19][20][21][22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%