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Dka Algorithm

Endocrine And Metabolic 2: Diabetic Ketoacidosis Portal

Endocrine And Metabolic 2: Diabetic Ketoacidosis Portal

Introduction DKA develops as a result of insufficient insulin activity and increased counter-regulatory hormones which result in accumulation of ketones (organic acids) and hyperglycemia. This hyperglycemia causes an osmotic diuresis leading to volume contraction and sodium/potassium losses. DKA is a serious complication with significant mortality for patients with insulin-dependent diabetes mellitus. Under certain stressful conditions (eg, MI or sepsis), even patients with non-insulin-dependent diabetes may develop DKA. Furthermore, DKA may often be the initial manifestation of diabetes, especially in pediatric patients.1 Patient Assessment History. Patients with DKA as the initial manifestation of diabetes often experience weight loss, polyuria, and polydipsia. Initial complaints include nausea, weakness, vomiting, and abdominal pain, (PEDS) particularly in children.1 The abdominal pain is usually vague and non-localized but can mimic an acute abdomen. Often, symptoms have progressed over several days. Other signs and symptoms are associated with the concurrent disease/stress event(s) that precipitated the DKA episode, such as infection (the most likely cause), cardiovascular events, stroke, trauma, pregnancy, and other severe stresses. A detailed history helps in managing this complex disorder. Exam. Patients with severe DKA may exhibit shock or altered level of consciousness/coma. Clinically, the patient is usually severely dehydrated; tachycardia is often present. Tachypnea/hyperventilation (Kussmaul respirations—deep, gasping) may be due to respiratory compensation for metabolic acidosis. Ketosis may cause acetone halitosis (a fruity odor on the breath). Other signs will accompany the associated conditions. Diagnostic Studies. An ECG is useful to identify MI if Continue reading >>

Treatment Of Diabetic Ketoacidosis In The Emergency Department Utilizing A Web Based Insulin Infusion Algorithm

Treatment Of Diabetic Ketoacidosis In The Emergency Department Utilizing A Web Based Insulin Infusion Algorithm

American Association of Clinical Endocrinologists (AACE) Annual Scientific & Clinical Congress Authors Joseph Aloi,1 Raymie McFarland,2 Margaret Bachand,3 Courtenay Harrison3 Ongoing efforts at improving quality metrics in the care of persons with diabetes frequently focus on avoiding unnecessary hospitalizations, decreasing length of stay and avoiding readmission to hospital following discharge. Our prior experience with Glucommander, a web based insulin dosing algorithm, in inpatient insulin protocols suggested that its use in the emergency department (ED) would be safe. We previously studied the effectiveness of the Glucommander system for the treatment of mild to moderate Diabetic Ketoacidosis (DKA) in the ED and reported early data on 15 patients. We now report a full 1 year experience with 35 patients studied. DKA is a frequent cause for hospital admissions – accounting for up to 8% of general medicine admissions in some hospital studies.4 Current standard treatment protocols involves use of intravenous insulin infusions monitored in the intensive care unit (ICU); raising both the cost and complexity of care. Methods 35 Patients seen in the ED diagnosed with DKA during the 2012 calendar year were reviewed. All patients were studied at a single site – Virginia Beach General Hospital (VGBH) a 300 bed community hospital within the Sentara healthcare system. Patients seen in the ED with either significant hyperglycemia (glucose >300 mg/dL) or DKA were placed on the Glucomander protocol. Patients were then monitored for readiness to be discharged or need for admission. Adult patients with blood glucose >250 mg/dL, a positive anion gap and/or ketonuria were eligible to participate. Patients with severe acidosis (pH <7.0 or serum bicarbonate <10 nmol/L), or a concomi Continue reading >>

#25: Master Hyperglycemia And Dka

#25: Master Hyperglycemia And Dka

Master the management of hyperglycemia, DKA, and learn to avoid common pitfalls. This episode is packed with clinical pearls from repeat guest, Endocrinologist, Dr. Jeffrey Colburn. Recommend a guest or topic and give feedback at [email protected] Rate us on iTunes. Clinical Pearls: Type 1 diabetes (DM1) occurs by autoimmune destruction of beta cells occurs at any age Typically lean body type and normal lipid profiles Type 2 diabetes (DM2) Typically obese and insulin resistant Eventually fat deposition in pancreas destroys insulin production 15-20 years after onset of DM2 leading to absolute insulin deficiency Triad of DKA = hyperglycemia, ketonemia, acidemia DKA occurs w/total lack of insulin leads to inability to utilize glucose (hyperglycemia) Simulated starvation occurs Counter regulatory hormones kick in Free fatty acids are broken down for fuel Keto acids are made as a by product (ketonemia) Acidemia occurs DKA can occur in DM2 if overwhelming infection, or infarction (MI or CVA) Even just a little bit of insulin can keep patient out of DKA! Dehydration is a cardinal issue in DKA from osmotic diuresis Often 6-8 liters depleted! Sick day rules for Type 1 diabetes Early contact with healthcare team Reduce, but do not discontinue insulin during the illness (see #8) Check frequent fingersticks Use antipyretics to manage fever Push the fluids Educate family members about signs/symptoms of DKA If sick, then drop basal insulin by 20% whether SQ or basal rate on insulin pump Keep mealtime insulin dose the same, but skip if not eating Ketones Beta hydroxybutyrate is the predominant ketone in DKA Urine ketones measure acetoacetate (strongly) and acetone (weakly) NOT beta hydroxybutyrate Serum ketones measure acetoacetate and acetone NOT beta hydroxybutyrate Thus, che Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diagnosis of DKA: � Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap � serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 2 Updated 05/02/17 DKA Diagnostic Criteria: � Blood glucose >250 mg/dl � Arterial pH <7.3 � Bicarbonate ≤18 mEq/l � Anion Gap Acidosis � Moderate ketonuria or ketonemia 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) 2. If serum K+ is <3.3 mEq/L hold insulin � Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I (*In PREGNANCY utilize OB DKA order set) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Insulin deficiency - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015, Revised DKA Workgroup 1_2016 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II *In PREGNANCY when sugar <200 proceed to OB DKA Phase II *PREGNANCY � Utilize OB DKA order set Phase 1 � When glucose reaches 200mg/dL, Initiate OB DKA Phase 2 � Glucose goals 100-150mg/dL OB DKA Phase 2 Determine hydration status Hypovolemic shock Mild hypotensio Continue reading >>

Emergency Department

Emergency Department

This is a CONTROLLED document for internal use only. Any documents appearing in paper form are not controlled and should be checked against the electronic file version prior to use. TITLE: GASHA Pediatric Diabetic Ketoacidosis (DKA) Physician and Nursing Protocol NUMBER: 1-450 Applies to: All Nursing Staff and Physicians Caring for Children with DKA POLICY Diabetic Ketoacidosis (DKA) involves a combination of hyperglycemia, acidosis, and ketones. It is diagnosed when: 1. the blood glucose is greater than or equal to 11 mmol/L 2. capillary pH is less than or equal to 7.3 and/or capillary bicarbonate is less than or equal to 15 mmol/L 3. ketones are present in the blood and/or urine (see below). It usually takes days to develop DKA, but it can take hours in children with acute illness, insulin omission or insulin pump failure. Causes of DKA Include: • undiagnosed type 1 diabetes • insulin omission or manipulation • inadequate insulin dosing and monitoring during periods that significantly increase insulin needs: (illness, infection, major stress, puberty, pregnancy) • insulin pump or infusion site malfunction or misuse Signs and symptoms Include: • polyuria • polydipsia • dehydration • weight loss • lethargy • nausea, vomiting and abdominal pain • fruity or acetone smelling breath • flushed face • confusion • hyperventilation and Kussmaul breathing (rapid, deep, sighing – mouth breathing) • ↑ heart rate and ↑ respirations, and ↓ blood pressure Acute dehydration must be treated with IV fluid replacement. Overhydration, correcting the hyperglycemia too quickly, the use of insulin in the first 1 – 2 hours of fluid therapy, and the use of bicarbonate ha Continue reading >>

M A N A G E M E N T A N D T R E A T M E N T O F

M A N A G E M E N T A N D T R E A T M E N T O F

This care process model (CPM) was developed by Intermountain Healthcare’s Pediatric Clinical Specialties Program. It provides guidance for identifying and managing type 1 diabetes in children, educating and supporting patients and their families in every phase of development and treatment, and preparing our pediatric patients to transition successfully to adulthood and adult diabetes self-management. This CPM is based on guidelines from the American Diabetes Association (ADA), particularly the 2014 position statement Type 1 Diabetes Through the Life Span, as well as the opinion of local clinical experts in pediatric diabetes.ADA1,CHI Pediatric Type 1 Diabetes C a r e P r o c e s s M o d e l F E B R U A R Y 2 0 1 7 2 0 17 U p d a t e Why Focus on PEDIATRIC TYPE 1 DIABETES? Diabetes in childhood carries an enormous burden for patients and their families and represents significant cost to our healthcare system. In 2008, Intermountain Healthcare published the first CPM on the management of pediatric diabetes with the overall goal of helping providers deliver the best clinical care in a consistent and integrated way. What’s new: • Separate CPMs for type 1 and type 2 pediatric diabetes to promote more- accurate diagnosis and more-focused education and treatment. • Updated recommendations for diagnostic testing, blood glucose control, and follow-up care specifically related to pediatric type 1 diabetes. • A more comprehensive view of treatment for pediatric type 1 diabetes — one that emphasizes psychosocial wellness for patient and family and lays a foundation for better health over the lifespan. • Information and tools to support pediatric type 1 diabetes care by nonspecialist providers — important for coping with the ongoin Continue reading >>

Chapter 11: Diabetic Ketoacidosis In Pregnancy

Chapter 11: Diabetic Ketoacidosis In Pregnancy

Despite recent advances in the evaluation and medical treatment of diabetes in pregnancy, diabetic ketoacidosis (DKA) remains a matter of significant concern. The fetal loss rate in most contemporary series has been estimated to range from 10% to 25%. Fortunately, since the advent and implementation of insulin therapy, the maternal mortality rate has declined to 1% or less. In order to favorably influence the outcome in these high-risk patients, it is imperative that the obstetrician/provider be familiar with the basics of the pathophysiology, diagnosis, and treatment of DKA in pregnancy. DKA is characterized by hyperglycemia and accelerated ketogenesis. Both a lack of insulin and an excess of glucagon and other counter-regulatory hormones significantly contribute to these problems and their resultant clinical manifestations. Glucose normally enters the cell secondary to the effects of insulin. The cell then may use glucose for nutrition and energy production. When insulin is lacking, glucose fails to enter the cell. The cell responds to this starvation by facilitating the release of counter-regulatory hormones, including glucagon, catecholamines, and cortisol. These counter-regulatory hormones are responsible for providing the cell with an alternative substrate for nutrition and energy production. By the process of gluconeogenesis, fatty acids from adipose tissue are broken down by hepatocytes to ketones (acetone, acetoacetate, and β-hydroxybutyrate [BHB] = ketone bodies), which are then used by the body cells for nutrition and energy production (Fig. 11-1). The lack of insulin also contributes to increased lipolysis and decreased reutilization of free fatty acids, thereby providing more substrate for hepatic ketogenesis. A basic review of the biochemistry involving D Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

University Of Zagreb

University Of Zagreb

SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 UNIVERSITY OF ZAGREB SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 This graduation paper has been completed at the Department of Paediatrics at the University Hospital Centre Zagreb (Rebro hospital) under the supervision of Dr. sc. Mario Ćuk and was submitted for evaluation during the academic year 2013 /2014. LIST OF TABLES Table 1: DKA laboratory diagnosis criteria Table 2: Classification of DKA. Modified from Kliegman et al. Nelson Textbook of Pediatrics, 2011. Table 3: Table 3: Summary of key data of patients admitted to pediatric ICU at Rebro hospital. LIST OF FIGURES Figure 1: DKA pathogenesis. Figure 2: Ketone bodies: showing formation of negatively charged conjugate bases of the ketoacids. The conjugate bases cause the increased anion gap in DKA metabolic acidosis. Figure 3: Algorithm of key steps in DKA pathophysiology. Colour coded to highlight the two areas that treatment should target: metabolic acidosis and hyperglycemia. Figure 4: True sodium level calculations for glucose levels above 100mg/dL (5.6mmol/L). Figure 5: Goals of DKA management Figure 6: Diabetic ketoacidosis treatment: Milwaukee protocol. Modified from Kliegman et al. Nelson Textbook of Paediatrics. 2011 p.1979 Figure 7: DKA incidence between 1 st January 2009 – 30 th June 2014. LIST OF ABBREVIATIONS DKA ..............Diabetic Ketoacidosis CE...................C Continue reading >>

A Unified Hyperglycemia And Diabetic Ketoacidosis (dka) Insulin Infusion Protocol Based On An Excel Algorithm

A Unified Hyperglycemia And Diabetic Ketoacidosis (dka) Insulin Infusion Protocol Based On An Excel Algorithm

Abstract: Objective – An insulin infusion protocol (IIP) was instituted in medical and surgical ICUs for post-cardiac surgery stress hyperglycemia (SH), diabetes hyperglycemia (DH), and DKA. Prior to 2014, Saint Louis University Hospital (SLUH) used a proportionate delivery protocol which required hourly Insulin Infusin Rate (IIR) recalculation based on BG change. A separate protocol was followed for diabetic ketoacidosis (DKA). A unified ICU protocol was designed in 2013 and implemented in 2014 for treatment of DH, DKA, and post-cardiothoracic surgery SH to meet SCIP criteria. The protocol utilized conventional diabetes management techniques, i.e. 1) body weight based, 2) designed with the concept of basal plus correction factor, 3) pre-calculated insulin doses , 4) maximum IIR at higher BG and 6) progressively decreasing IIR as BG approaches designated target range (DTR) to limit hypoglycemia Method - The IIP was assessed during one month for all patients in ICUs. The IIP was developed in Excel and our project is IRB exempt. The IIR is higher at BG >160mg/dL (0.5units/ kg/24 hour, defined as “Phase 1” to lower hyperglycemia), and decreases progressively as BG decline. There is an abrupt decrease in the IIR at a threshold BG of 160mg/dL, (rate 0.3units/kg/ 24hours defined as “Phase 2”, maintenance rate) to sustain BG between a DTR, 120 mg/dL-180 mg/dL. An acceptable target range (ATR) is considered between 100mg/dL-200mg/dL. A correction factor for BG >120mg/dL is added to the IIR by estimating Total Daily Dose (TDD) of insulin. IIR is pre-calculated and stored in the electronic medical record system (EPIC) in weight based columns from 40kg through 150kg with increments of 10 kg. Nurses titrate IIR hourly based only on the current BG. When BG has been in targ Continue reading >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Children's Hospital Of Philadelphia

Children's Hospital Of Philadelphia

If you have questions about any of the clinical pathways or about the process of creating a clinical pathway please contact us. ©2017 by Children's Hospital of Philadelphia, all rights reserved. Use of this site is subject to the Terms of Use. The clinical pathways are based upon publicly available medical evidence and/or a consensus of medical practitioners at The Children’s Hospital of Philadelphia (“CHOP”) and are current at the time of publication. These clinical pathways are intended to be a guide for practitioners and may need to be adapted for each specific patient based on the practitioner’s professional judgment, consideration of any unique circumstances, the needs of each patient and their family, and/or the availability of various resources at the health care institution where the patient is located. Accordingly, these clinical pathways are not intended to constitute medical advice or treatment, or to create a doctor-patient relationship between/among The Children’s Hospital of Philadelphia (“CHOP”), its physicians and the individual patients in question. CHOP does not represent or warrant that the clinical pathways are in every respect accurate or complete, or that one or more of them apply to a particular patient or medical condition. CHOP is not responsible for any errors or omissions in the clinical pathways, or for any outcomes a patient might experience where a clinician consulted one or more such pathways in connection with providing care for that patient. Continue reading >>

Diabetic Ketoacidosis Mortality Prediction Model (dka Mpm) Score

Diabetic Ketoacidosis Mortality Prediction Model (dka Mpm) Score

Note: This calculator is not externally validated and should be used with caution. It is not intended to routinely disposition patients. The APACHE II Score may be a better mortality predictor. Use in patients with DKA. Continue reading >>

Hyperglycemic Crises In Adult Patients With Diabetes

Hyperglycemic Crises In Adult Patients With Diabetes

Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are the two most serious acute metabolic complications of diabetes. DKA is responsible for more than 500,000 hospital days per year (1,2) at an estimated annual direct medical expense and indirect cost of 2.4 billion USD (2,3). Table 1 outlines the diagnostic criteria for DKA and HHS. The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA. HHS is characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of significant ketoacidosis. These metabolic derangements result from the combination of absolute or relative insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Most patients with DKA have autoimmune type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness such as trauma, surgery, or infections. This consensus statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS in adult subjects. It is based on a previous technical review (4) and more recently published peer-reviewed articles since 2001, which should be consulted for further information. Recent epidemiological studies indicate that hospitalizations for DKA in the U.S. are increasing. In the decade from 1996 to 2006, there was a 35% increase in the number of cases, with a total of 136,510 cases with a primary diagnosis of DKA in 2006—a rate of increase perhaps more rapid than the overall increase in the diagnosis of diabetes (1). Most patients with DKA were between the ages of 18 and 44 years (56%) and 45 and 65 years (24%), with only 18% of patie Continue reading >>

Canine Diabetic Ketoacidosis

Canine Diabetic Ketoacidosis

Use this algorithm to diagnose and treat diabetic ketoacidosis in dogs. CANINE DIABETIC KETOACIDOSIS • Alice Huang & J. Catharine Scott-Moncrieff Material from Clinician’s Brief may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us. Continue reading >>

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