Standardized Hospital Management of Pediatric Diabetic Ketoacidosis Reduces Frequency of Low Blood Glucose Episodes

2021 ◽  
Author(s):  
Peter M. Wolfgram ◽  
Mogen Frenkel ◽  
Pamela Gage ◽  
Rebecca Sprague ◽  
Ashley Servi ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Hospital Management

Standardizing Hospital Management of Pediatric Diabetic Ketoacidosis in order to Reduce Iatrogenic Low Blood Glucose Episodes

2021 ◽  
Author(s):  
Mogen Frenkel ◽  
Shannon H. Baumer-Mouradian ◽  
Ashley Servi ◽  
Pamela Gage ◽  
Rebecca Sprague ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Hospital Management

scholarly journals 30 Reducing iatrogenic low blood glucose episodes during hospital management of pediatric diabetic ketoacidosis

2019 ◽  
Author(s):  
Shannon Baumer-Mouradian ◽  
Ashley Servi ◽  
Pam Gage ◽  
Sandy Huitink ◽  
Rebecca Sprague ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Hospital Management

An Approach to diabetic ketoacidosis in an emergency setting.

2020 ◽  
Vol 15 ◽  
Author(s):  
Dario Pitocco ◽  
Mauro Di Leo ◽  
Linda Tartaglione ◽  
Emanuele Gaetano Rizzo ◽  
Salvatore Caputo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Blood Glucose Concentration ◽  
Diabetic Complication ◽  
Emergency Setting ◽  
Online Activity

Background: Diabetic Ketoacidosis (DKA) is one of the most commonly encountered diabetic complication emergencies. It typically affects people with type 1 diabetes at the onset of the disease. It can also affect people with type 2 diabetes, although this is uncommon. Methods: Research and online content related to diabetes online activity is reviewed. DKA is caused by a relative or absolute deficiency of insulin and elevated levels of counter regulatory hormones. Results: Goals of therapy are to correct dehydration, acidosis and to reverse ketosis, gradually restoring blood glucose concentration to near normal. Conclusion: Furthermore it is essential to monitor potential complications of DKA and if necessary, to treat them and any precipitating events.

scholarly journals Outcome of the use of 0.9% saline versus 0.45% saline for fluid rehydration in moderate and severe diabetic ketoacidosis in children

2021 ◽  
Vol 69 (1) ◽  
Author(s):  
Nora El Said Badawi ◽  
Mona Hafez ◽  
Heba Sharaf Eldin ◽  
Hend Mehawed Abdelatif ◽  
Shimaa Atef ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Normal Saline ◽  
Sodium Concentration ◽  
Saline Group ◽  
Serum Electrolytes ◽  
Serum Chloride ◽  
Significant Difference ◽  
Rehydration Solution ◽  
The Moment

Abstract Background The debate for the optimum sodium concentration in the rehydration solution in diabetic ketoacidosis (DKA) persists till the moment. The aim was to compare the outcome of 0.9% saline versus 0.45% saline in children with moderate and severe (DKA) regarding the effect on serum electrolytes, duration of DKA resolution and the incidence of hyperchloremia. Results A retrospective analysis of 121 children with moderate or severe DKA was done. After the initial 4 h in which both groups received normal saline, patients were divided into two groups continuing on 0.9% (N=72) or switched to 0.45% saline (N=49). Serum chloride and Cl/Na ratios were significantly higher in 0.9% saline group at 4 and 8 h. The 0.9% saline group had significantly higher proportion of hyperchloremia at 4 and 8 h (P value: 0.002, 0.02). The median duration of correction of DKA (14 h among 0.9% saline versus 10 h among 0.45% saline) without significant difference (P value= 0.43). The change in plasma glucose, effective osmolarity, corrected Na levels were comparable between groups. Conclusion There is an unavoidable iatrogenically induced rise in serum chloride with higher incidence of hyperchloremia with the use of normal saline in rehydration of children presenting in DKA and shock. The use of 0.45% saline as post-bolus rehydration fluid is not associated with a decline in the corrected serum sodium concentration and does not affect the rate of correction of acidosis or rate of drop in blood glucose or duration of DKA resolution when compared to normal saline.

scholarly journals Euglycemic Diabetic Ketoacidosis in Pregnancy: A Case Report and Review of Current Literature

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Johnny F. Jaber ◽  
Matthew Standley ◽  
Raju Reddy
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Case Reports ◽  
Anion Gap ◽  
Fetal Mortality ◽  
Glucose Levels ◽  
Elevated Glucose ◽  
High Doses ◽  
Euglycemic Diabetic Ketoacidosis ◽  
In Pregnancy

Diabetic ketoacidosis (DKA) in pregnancy is associated with high fetal mortality rates. A small percentage of DKA occurs in the absence of high glucose levels seen in traditional DKA. Prompt recognition and management is crucial. We report a case of a 30-year-old pregnant woman with type 1 diabetes mellitus admitted with euglycemic DKA (blood glucose <200 mg/dL). Initial laboratory testing revealed a severe anion gap acidosis with pH 7.11, anion gap 23, elevated β-hydroxybutyric acid of 9.60 mmol/L, and a blood glucose of 183 mg/dL—surprisingly low given her severe acidosis. The ketoacidosis persisted despite high doses of glucose and insulin infusions. Due to nonresolving acidosis, her hospital course was complicated by spontaneous intrauterine fetal demise. Euglycemia and severe acidosis continued to persist until delivery of fetus and placenta occurred. It was observed that the insulin sensitivity dramatically increased after delivery of fetus and placenta leading to rapid correction of ketoacidosis. This case highlights that severe ketonemia can occur despite the absence of severely elevated glucose levels. We discuss the mechanism that leads to this pathophysiologic state and summarize previously published case reports about euglycemic DKA in pregnancy.

scholarly journals 345. Acute Onset Diabetic Ketoacidosis/Hyperosmolar Hyperglycemic State in Patients Taking Integrase Strand Transfer Inhibitors

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S183-S184 ◽  
Author(s):  
Afua Duker Ntem-Mensah ◽  
Nina Millman ◽  
Niyati Jakharia ◽  
Amanda Theppote ◽  
Mona-Gekanju Toeque ◽  
...  
Keyword(s):  
Weight Gain ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Diabetic Ketoacidosis ◽  
Glucose Level ◽  
Case Reports ◽  
Acute Onset ◽  
Anion Gap ◽  
Hyperosmolar Hyperglycemic State ◽  
Hba1c Levels

Abstract Background A few case reports have noted uncontrolled hyperglycemia in patients switched to dolutegravir. Several cohort studies have found increased weight gain among patients treated with integrase inhibitors (INSTI). We present clinical observations among 3 patients admitted to hospital for diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) while receiving INSTIs for the management of HIV. Methods Case 1: A 44-year-old man with HIV and dyslipidemia presented with altered mental status and lethargy. A fingerstick glucose was >600 mg/dL. Chemistries revealed glucose of 1,600 mg/dL and an elevated β-hydroxybutyrate. HbA1c was 12.4%. His antiretroviral regimen consisted of cEVG/TAF/FTC for the last 3 years. Previous HbA1c levels were 5.7% and 6.2% (Figure 1). Case 2: A 55-year-old woman with HIV, hypertension, dyslipidemia, and obesity presented with polyuria and polydipsia. The blood glucose level was >1,200 mg/dL with an anion gap >30 and HbA1c of 15%. Previous HbA1c levels ranged between 5.6 and 5.8% (Figure 2). She had been taking ABC/FTC/DTG for 2 years. Case 3: A 64 yo man with a history of HIV, hypertension, and obesity presented with polyuria and polydipsia. The blood glucose level was 1,152 mg/dL with no anion gap and HbA1c of 13.4%. Six months before, he had been switched from a c/DRV- based ART regimen to ABC/FTC/DTG. Previous HbA1c levels ranged between 5.8% and 6.2% (Figure 3). Results Discussion: In the first 2 patients, the presentation with acute onset DKA occurred more than a year after being on an INSTI-based regimen; however, the latter patient presented with HHS within 6 months of being switched to an INSTI-containing regimen. The mechanism of action of INSTIs causing weight gain or an association with hyperglycemia is still under investigation. Conclusion Although the temporal onset of DKA and HHS while receiving INSTIs was not precise, the possible association of INSTIs and their direct effects on insulin resistance and diabetes warrant additional attention from post-market data. Meanwhile, providers should monitor INSTI-treated patients closely, especially those with features of metabolic syndrome. Disclosures All authors: No reported disclosures.

scholarly journals Usefulness of a blood glucose and ketone monitoring device as a screening tool for lethal diabetic ketoacidosis

2020 ◽  
Vol 135 (1) ◽  
pp. 293-299
Author(s):  
Pierre-Antoine Peyron ◽  
Maëlle Plawecki ◽  
Maisy Lossois ◽  
Manuela Lotierzo ◽  
Eric Baccino ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Screening Tool ◽  
Monitoring Device

scholarly journals MON-LB119 Euglycemic Diabetic Ketoacidosis in a Patient on Canagliflozin Presenting With Hypoglycemia

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sindhura Inkollu ◽  
Sindhuja Korem ◽  
Sudha Ganne
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Mental Status ◽  
Altered Mental Status ◽  
Sglt2 Inhibitors ◽  
Anion Gap ◽  
Hypoglycemic Agents ◽  
Tract Infections ◽  
Euglycemic Diabetic Ketoacidosis

Abstract Background: Sodium glucose co-transporter 2 (SGLT-2) inhibitors are newer class of antihyperglycemics that cause reversible inhibition of the sodium-glucose cotransporters in the renal proximal tubules resulting in increased urinary glucose. Common side effects include yeast and urinary tract infections. The US Food and Drug Administration issued a safety warning pertaining to the development of diabetic ketoacidosis (DKA) with the use of SGLT2 inhibitors. The mechanisms by which SGLT2 inhibitors cause euglycemic DKA are unclear. SGLT2 inhibitors may lead to a decrease in either endogenous or exogenous insulin and an increase in glucagon production.1 This insulin deficiency or resistance may be mild in Type 2 diabetics, however, preventing the profound spike in blood glucose seen in traditional DKA. Here, we report a case of euglycemic DKA in a patient on Canagliflozin who presented initially with hypoglycemia. Clinical case: A 70 year old female presented with altered mental status for 1 day duration. Her past medical history is significant for type 2 Diabetes Mellitus, being managed on Canagliflozin, Glimepiride and Janumet. One week prior to admission she had lumbar spinal fusion surgery. Since then she has been feeling weak and tired with poor oral intake, but continued to use her medications. Initial laboratory findings showed blood glucose of 68 (70-100 mg/dl) without any acidosis. Her altered mental status was attributed to higher opioid doses which she received prior. Oral hypoglycemic agents have been held. On 2nd day of hospitalization, patient became more lethargic and complained of nausea. Laboratory testing revealed a serum glucose of 250mg/dL, serum bicarbonate of 13 (21–31mmol/L), and Anion gap of 25 (3.6–11.0mmol/L). With the suspicion of DKA, a beta-hydroxy butyrate level was obtained which was elevated at 90.10 (0 – 4.16 mg/dL). Venous blood gas analysis was significant for pH 7.23 (7.31-7.41) and pCO2 – 28 (41-51 mmHg). Urinalysis showed ketosis and glucosuria. Patient was diagnosed as euglycemic diabetic ketoacidosis from Canagliflozin in presence of precipitating factors - stress and poor intake. Patient was treated with insulin drip and intravenous fluids with reduction in anion gap and correction of acidosis within 24hrs. There was a gradual improvement in her mental status. She was discharged on subcutaneous insulin, and all other diabetic medications were stopped. Conclusion: Our case highlights the importance of being vigilant in a patient on Canagliflozin, euglycemic DKA can occur even if they present initially with hypoglycemia and no acidosis. Reference: 1. Ogawa W, Sakaguchi K. Euglycemic diabetic ketoacidosis induced by SGLT2 inhibitors: possible mechanism and contributing factors. J Diabetes Investig. 2016;7(2):135-138.

scholarly journals MON-675 Ziprasidone Induced Diabetic Ketoacidosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Varshitha Thanikonda ◽  
Fatima Jalil ◽  
Vitaly Kantorovich
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Atypical Antipsychotic ◽  
Atypical Antipsychotics ◽  
Sugar Content ◽  
Dry Mouth ◽  
Close Monitoring ◽  
Antipsychotic Therapy ◽  
Increased Risk

Abstract Introduction: Atypical antipsychotics are known to cause increased risk of type 2 Diabetes Mellitus (DM2), dyslipidemia, and weight gain (metabolic syndrome). Clozapine, a commonly used anti-psychotic, is known to cause Diabetic Ketoacidosis (DKA), but literature has rarely shown an association of DKA with Ziprasidone. Case: A 42-year-old African American female presented with two weeks of polyuria, polydipsia, 23-pound weight loss, blurriness of vision, and dry mouth. Before the presentation, she had been drinking several drinks with high sugar content. Her medications included Ziprasidone (Geodon), Trileptal, and Cogentin for her bipolar disorder. She was started on Ziprasidone in 2007, changed to Brand name Geodon in 2014. Except for dry mouth, her exam was unremarkable. Labs were significant for blood glucose of 1114 mg/dL, bicarbonate of 18mmol/L, beta-hydroxybutyrate of 3.33 mmol/L, serum osmolality of 334 mOsm/kg. She was diagnosed with new-onset diabetes mellitus presenting as diabetic ketoacidosis. Her mother was diagnosed with DM2 in her 40s. She ha difficult to control blood sugars despite aggressive hydration and required regular insulin drip for 3 days for her anion gap to close. Managing her BGs was challenging. Discussion: Clozapine and olanzapine are the common atypical antipsychotics that can cause DKA1, 2. To our knowledge, Ziprasidone is associated with hyperglycemia within days of starting the drug and HHS but not with DKA. For atypical antipsychotic associated DKA, risk factors include the duration of antipsychotic therapy, polypharmacy with multiple antipsychotic agents, non-Caucasians, obesity and pre-diabetes2, 3. Proposed mechanisms include peripheral insulin resistance, alteration of pancreatic beta-cell function by inhibiting 5-HT1A/2A/2C and alpha 2 adrenergic receptors1-3. However, there is no explanation of why few people develop complications while others do not. There is hypothesis regarding leptin gene polymorphisms of receptors that may play a role4. While starting patients on Ziprasidone, close monitoring of blood glucose is necessary before initiation and regular follow up thereafter3. 1. Henderson DC. Atypical antipsychotic-induced diabetes mellitus: How strong is the evidence? CNS Drugs. 2002. 2. Vuk A. Diabetic ketoacidosis associated with antipsychotic drugs: Case reports and a review of literature. Psychiatr Danub. 2017. 3. Schwenkreis P. Atypical antipsychotics and diabetes mellitus. World J Biol Psychiatry. 2004. 4. 1. Reynolds GP. Metabolic side effects of antipsychotic drug treatment - pharmacological mechanisms. Pharmacol Ther. 2010.

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