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End-Stage Renal Disease Increases Rates of Adverse Glucose Events When Treating Diabetic Ketoacidosis Or Hyperosmolar Hyperglycemic State Caitlin M

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End-Stage Renal Disease Increases Rates of Adverse Glucose Events When Treating Diabetic Ketoacidosis Or Hyperosmolar Hyperglycemic State Caitlin M Clinical Diabetes Papers in Press, published online May 3, 2017 End-Stage Renal Disease Increases Rates of Adverse Glucose Events When Treating Diabetic Ketoacidosis or Hyperosmolar Hyperglycemic State Caitlin M. Schaapveld-Davis,1 Ana L. Negrete,1,2 Joanna Q. Hudson,1–3 Jagannath Saikumar,3 Christopher K. Finch,1,2 Mehmet Kocak,4 Pan Hu,4 and Megan A. Van Berkel,1,2 FEATURE ARTICLE FEATURE ■ IN BRIEF Treatment guidelines for diabetic emergencies are well described in patients with normal to moderately impaired kidney function. However, management of patients with end-stage renal disease (ESRD) is an ongoing challenge. This article describes a retrospective study comparing the rates of adverse glucose events (defined as hypoglycemia or a decrease in glucose >200 mg/dL/hour) between patients with ESRD and those with normal kidney function who were admitted with diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS). These results indicate that current treatment approaches to DKA or HHS in patients with ESRD are suboptimal and require further evaluation. anagement strategies for dia- den, characterized by an exchange of betic ketoacidosis (DKA) and the intracellular potassium ion pool Mhyperosmolar hyperglycemic for the newly increased extracellular state (HHS) are well established in hydrogen ion concentration (1–3). patients with normal kidney function. In contrast, patients with ESRD and Therapy typically includes aggressive DKA or HHS are routinely observed fluid resuscitation, electrolyte replace- to have hyperkalemia resulting from ment, insulin administration, and a combination of transcellular shifts treatment of the precipitating cause and a lack of renal clearance, thus (if identified). However, treatment eliminating the need for electrolyte strategies for these key principles replacement (4). may differ for patients with DKA or In patients with ESRD and DKA HHS and severe kidney dysfunction or HHS, adjustments in insulin (1–3). For example, aggressive fluid administration may be warranted. 1Methodist University Hospital, Memphis, TN resuscitation in a patient with end- Normally, insulin is primarily metab- 2University of Tennessee Health and Science stage renal disease (ESRD) is com- olized into useful amino acids by Center College of Pharmacy, Memphis, TN plicated by the risk of developing the kidneys’ proximal tubular cells. 3 University of Tennessee Health and or furthering significant pulmonary Insulin gains access to these cells Science Center College of Medicine, edema and uncontrolled hypertension through two mechanisms: 1) glomer- Memphis, TN (4). In addition to intravascular fluid ular filtration followed by luminal 4University of Tennessee Department of depletion, patients with normal kid- reabsorption and 2) diffusion through Preventative Medicine, Memphis, TN ney function who suffer from DKA or peritubular capillary membranes Corresponding author: Megan A. Van HHS frequently have reduced total- and ensuing binding to basolateral Berkel, [email protected] body potassium, despite normal or membranes of tubular cells (5,6). https://doi.org/10.2337/cd16-0060 elevated serum measurements. This Therefore, in patients with impaired metabolic derangement often stems kidney function, delayed insulin ©2017 by the American Diabetes Association. Readers may use this article as long as the work from the combination of the hemo- clearance can complicate titration of is properly cited, the use is educational and not concentrating effect of osmotic di- the continuous insulin infusion and for profit, and the work is not altered. See http:// creativecommons.org/licenses/by-nc-nd/3.0 uresis and an inherent mechanism of increase the risk of rapid decreases for details. reducing the patient’s acidotic bur- in blood glucose and consequent CLINICAL DIABETES 1 Clinical Diabetes Online Ahead of Print, published online May 3, 2017 FEATURE ARTICLE Clinical Diabetes Papers in Press, published online May 3, 2017 hypoglycemic events (7,8). Rapid Science Center institutional review serum bicarbonate level ≥15 mEq/L, reductions in blood glucose alter board. venous pH >7.3, or a calculated anion serum tonicity and osmolality, which Patients with ESRD with docu- gap ≤12 mEq/L. Resolution of HHS can place patients at an increased mentation of chronic hemodialysis was defined as normal osmolality risk of neurological sequelae such as (HD) were compared to a control (278–300 mOsm/kg), glucose <300 seizures or cerebral edema (3,4,9). group of patients with normal kid- mg/dL, and recovery of normal men- In patients with normal kidney ney function. Chronic HD was tal status (1,2). Mental status is very function, low-dose insulin drips are defined as scheduled HD for at least subjective and not always consistently expected to decrease serum glucose 3 months before admission. Patients charted, so objective data such as by approximately 50–70 mg/dL/hour, were included in the control group serum osmolality had to be used in but no study has demonstrated an if they presented to the emergency some cases for clearing of HHS. analogous correlation in the decline department with DKA or HHS Secondary outcomes were to of glucose in patients with severely and had a documented estimated evaluate differences in insulin impaired kidney function (1,2). glomerular filtration rate (eGFR) administration, fluid, and electro- These variations in insulin kinet- ≥60 mL/min/1.73 m2 (calculated lyte replacement for up to 24 hours ics in patients with ESRD present with the Modified Diet of Renal or until the resolution of DKA or clinicians with an additional chal- Disease Study equation) within 24 HHS. Additionally, hospital length of lenge when determining an insulin hours of hospital presentation (11). stay (LOS), intensive care unit (ICU) dosing regimen to achieve target To achieve a homogenous patient LOS, and time to resolution of DKA glucose levels. Despite these added population within the cohorts and or HHS were evaluated. Serum tonic- complications of DKA or HHS man- control for the effects of HD on ity was calculated as follows: agement in patients with ESRD, only DKA resolution, patients with stages case reports are available to describe I–IV of chronic kidney disease and 2 × [(serum sodium concentration) 2 treatment approaches (4,10). This an eGFR <60 L/min/1.73 m were + (serum glucose concentration)] not included. Patients were excluded retrospective study was designed to Secondary outcomes were also compare the DKA and HHS treat- if they received cardiopulmonary resuscitation or had a withdrawal stratified by early and late inpatient ment practices and safety outcomes HD, compared to patients with nor- of patients with ESRD to those of of care within 24 hours of hospital presentation, were transferred from mal kidney function. Early inpatient patients without significant kidney HD was defined as initiation of HD impairment. an outside facility, receive peritoneal dialysis, or had incomplete data as ≤12 hours after hospital presentation Materials and Methods determined by the primary investi- and late inpatient HD was defined as This was a multicenter, retrospective gator (e.g., no weight documented or HD initiation >12 hours after hos- study that evaluated adult patients lack of charting of rate changes for pital presentation. The cutoff of 12 who presented with DKA or HHS to the insulin drip). hours was chosen to represent the the emergency department of one of The primary objective of this average time to resolution of DKA or four hospitals within a single health study was to compare the rate of HHS in patients with normal kidney care system between September 2011 adverse glucose events (AGEs) function (12). and December 2014. Patients had to among patients with ESRD to that Statistical Analysis receive at least 1 hour of continu- of patients with normal kidney func- Descriptive statistics were provided as ous intravenous insulin infusion to tion. AGEs were defined as a blood frequency (percentages) for categor- be eligible for inclusion. Diagnoses glucose <70 mg/dL or a decrease ical variables and mean ± standard of DKA or HHS were identified by of >200 mg/dL in a 1-hour period. deviation (SD) or median (25–75% International Classification of Diseases Blood glucose levels were recorded interquartile range (IQR), as ap- 9th edition codes and independently and evaluated for hypoglycemia from propriate, for continuous variables. verified by the primary investigator hospital admission until 24 hours The association between categorical using objective diagnostic criteria after admission or until the resolution variables of interest was investigat- based on the American Diabetes of DKA or HHS, whichever was lon- ed using a χ2 test or Fisher’s exact Association (ADA) 2009 guidelines ger. A rapid decrease in blood glucose test, as appropriate. Distribution of (1), and analysis of available labo- was defined as >200 mg/dL/hour to continuous variables was compared ratory measurements (i.e., arterial assess patients at increased risk for via a Wilcoxon-Mann-Whitney test. pH, presence of ketones, anion gap, adverse neurological sequelae (3,4,9). The primary response variable was serum bicarbonate, and serum osmo- Resolution of DKA was defined as the likelihood of AGEs. Associations lality). The study was approved by blood glucose <200 mg/dL and two with categorical and continuous the University of Tennessee Health of the following clinical criteria: predictors of interest were explored 2 CLINICAL.DIABETESJOURNALS.ORG Clinical Diabetes Online
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