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Dka Algorithm

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 >>

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 >>

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

1. IV Isotonic Crystalloid Therapy • Shock fluid therapy is warranted if cardiovascular instability is present: Full shock dose of fluids is 90 mL/kg; start with ¼ to 1/3 dose and reassess until stable • Correct dehydration, provide maintenance needs, and replace ongoing losses over 6 to 24 hours: - % dehydration × body weight (kg) × 1000 plus - 20 mL/kg/day (insensible losses) plus - 20 to 40 mL/kg/day (maintenance sensible losses) plus - Account for vomiting, diarrhea, & polyuria (ongoing sensible losses) Alice Huang, VMD, & J. Catharine Scott-Moncrieff, Vet MB, MS, MA, Diplomate ACVIM & ECVIM Purdue University Canine Diabetic Ketoacidosis D i a gno s t i c Tre e / ENDOCRINOLOGY Peer Reviewed Physical Examination • Polyuria • Weight loss • Polydipsia • Vomiting • Polyphagia • Lethargy Patient may have only 1 or more of these signs. Laboratory Results • Blood glucose (BG): Hyperglycemia (> 200 mg/dL) • Blood gas (venous or arterial): Metabolic acidosis • Urine dipstick: Glucosuria; ketonuria or ketonemia Serum ketones can be measured if urine is unavailable. Diabetic Ketoacidosis Treatment 2. Electrolyte Supplementation (see Table 1, page 70) • Monitor serum potassium Q 4–6 H until within reference interval and stable; then Q 12–24 H • Monitor serum phosphorus Q 4–6 H until > 1.5; then Q 6–24 H • When supplementing potassium and phosphorus concurrently, take into account the amount of potassium contained in the potassium phosphate • Consider magnesium supplementation in instances of refractory hypokalemia 3. Regular Insulin • Continuous rate infusion (CRI) protocol:1 - Add 2.2 U/kg of regular insulin to 250 mL of 0.9% saline - Allow 50 Continue reading >>

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

Précis 1. Clinical setting—Any altered state of well being in the context of signifi cant hyperglycemia in a patient with type 1 (DKA) or advanced type 2 diabetes mel- litus (DKA or HHS), particularly during acute illness, may signify one of these diabetic emergencies. 2. Diagnosis (a) History: Most patients with diabetic ketoacidosis (DKA) or with hyperos- molar hyperglycemic state (HHS) will have a history of diabetes, and a his- tory of altered insulin dose, infection, signifi cant medical “stressâ€. Antecedent symptoms of polyuria and polydipsia, lassitude, blurred vision, and mental status changes may predominate the clinical picture. With DKA, abdominal pain and tachypnea are often present. (b) Physical examination usually reveals an altered sensorium, signs of volume contraction/dehydration (tachycardia, hypotension, dry mucus membranes, “tenting†of the skin); in DKA, the odor of acetone in the breath. (c) Laboratory evaluation. The diagnostic criteria for DKA include blood glu- cose above 250 mg/dL, arterial pH < 7.30, serum bicarbonate < 15 mEq/l Chapter 2 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Beatrice C. Lupsa and Silvio E. Inzucchi B. C. Lupsa , M.D. (*) • S. E. Inzucchi , M.D. Section of Endocrinology , Yale University School of Medicine , Yale-New Haven Hospital, 333 Cedar Street, FMP 107 , P.O. Box 208020 , New Haven , CT 06520 , USA e-mail: [email protected] 16 and moderate degree of ketonemia and/or ketonuria. Patients with HHS present with extreme hyperglycemia (blood glucose > 600 mg/dL), increased osmolality (> 320 mOsm/kg) and profound dehydration/volume contrac- tion. The laboratory evaluation of a patient with hyperglycemic emergency should include measurement of blood glucose and he 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 >>

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 >>

Use Of A Computer-based Insulin Infusion Algorithm To Treat Diabetic Ketoacidosis In The Emergency Department

Use Of A Computer-based Insulin Infusion Algorithm To Treat Diabetic Ketoacidosis In The Emergency Department

Abstract Background: Efforts at improving quality metrics in diabetes focus on minimizing adverse events and avoiding re-admissions to the hospital. Our experience with Glucommander™ (Glytec, Greenville, SC), a cloud-based insulin management software system, suggested that its use in the emergency department (ED) would be useful in treating patients with mild diabetic ketoacidosis (DKA). Materials and methods: Thirty-five patients seen in the ED with hyperglycemic crises and diagnosed with DKA during one calendar year were reviewed. A retrospective chart review was performed on patients who were placed on Glucommander™ for DKA management. We excluded patients with significant acidosis or concomitant medical illnesses. Results: Initial average capillary glucose level was 487 ± 68 mg/dL, average time to target glucose was 5 h 11 min, and rate of hypoglycemia (blood glucose level <70 mg/dL) was less than 0.3%. Sixteen patients treated with the protocol were discharged from the ED directly, and 19 were admitted. Patients were maintained for an average of 14 ± 1 h on the Glucommander™ protocol. There was a significantly higher anion gap (P = 0.002) and lower serum bicarbonate level (P = 0.006) in the admitted group. We found very low evidence of re-admission (6%) within 30 days of discharge from the ED for DKA patients. No significant glucose-related adverse events were noted. Conclusions: Use of Glucommander™ for guiding the insulin treatment of mild DKA in the ED can decrease admissions to the hospital for DKA by 45%. Low rates of hypoglycemia make this an option to improve efficiency of utilization of inpatient hospital beds. The cost savings for nonadmissions were estimated at $78,000 over the 12 months of the study. Our results suggest that Glucommander™ is 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 >>

Diabetic Ketoacidosis In Type 1 And Type 2 Diabetes Mellitusclinical And Biochemical Differences

Diabetic Ketoacidosis In Type 1 And Type 2 Diabetes Mellitusclinical And Biochemical Differences

Background Diabetic ketoacidosis (DKA), once thought to typify type 1 diabetes mellitus, has been reported to affect individuals with type 2 diabetes mellitus. An analysis and overview of the different clinical and biochemical characteristics of DKA that might be predicted between patients with type 1 and type 2 diabetes is needed. Methods We reviewed 176 admissions of patients with moderate-to-severe DKA. Patients were classified as having type 1 or type 2 diabetes based on treatment history and/or autoantibody status. Groups were compared for differences in symptoms, precipitants, vital statistics, biochemical profiles at presentation, and response to therapy. Results Of 138 patients admitted for moderate-to-severe DKA, 30 had type 2 diabetes. A greater proportion of the type 2 diabetes group was Latino American or African American (P<.001). Thirty-five admissions (19.9%) were for newly diagnosed diabetes. A total of 85% of all admissions involved discontinuation of medication use, 69.2% in the type 2 group. Infections were present in 21.6% of the type 1 and 48.4% of the type 2 diabetes admissions. A total of 21% of patients with type 1 diabetes and 70% with type 2 diabetes had a body mass index greater than 27. Although the type 1 diabetes group was more acidotic (arterial pH, 7.21 ± 0.12 vs 7.27 ± 0.08; P<.001), type 2 diabetes patients required longer treatment periods (36.0 ± 11.6 vs 28.9 ± 8.9 hours, P = .01) to achieve ketone-free urine. Complications from therapy were uncommon. Conclusions A significant proportion of DKA occurs in patients with type 2 diabetes. The time-tested therapy for DKA of intravenous insulin with concomitant glucose as the plasma level decreases, sufficient fluid and electrolyte replacement, and attention to associated problems remai Continue reading >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis is a complication of new or existing Type 1 Diabetes. Pediatric DKA may be complicated by cerebral edema and due to this risk, is treated differently than adult DKA. Health care providers must follow a published pediatric-specific protocol when treating pediatric DKA. We have chosen 3 examples of such protocols: a general treatment algorithm from the Canadian Diabetes Association, a detailed treatment algorithm from BC Children's Hospital (English) and a detailed treatment algorithm from Centre hospitalier universitaire Sainte-Justine (French). Each pediatric hospital in Canada will have a protocol that they follow, thus early communication with the diabetes specialist at your pediatric referral site is a key element of the management of these patients. Continue reading >>

Dka Without The Icu

Dka Without The Icu

As we discussed yesterday, the treatment algorithm for DKA is fairly straightforward with a few subtleties we rarely appreciate, until now. Yesterday we focused on fluids, today we move on to the insulin. Can we offer the patient anything else beside an insulin drip? Obviously the answer is yes, or else this pearl wouldn’t exist. In 2004, Umpierrez et al conducted an RCT of 20 patients comparing subcutaneous lispro (0.3U/kg bolus followed by 0.1U/kg/h) vs. an IV insulin (0.1 u/kg bolus followed by 0.1 U/kg/h drip). They found that there was no difference in time to correction of hyperglycemia, time to resolution of DKA, length of hospital stay, or rates of hypoglycemia. Later that year, they conducted a second study of 45 patients comparing doses of 0.1U/kg/h subcutaneous insulin to 0.2U/kg/h subcutaneous insulin to standard therapy. Not surprisingly, they showed that no protocol was more efficacious than another, however they did show a 39% high hospitalization charges in the IV insulin group due to the ICU setting necessary to manage the insulin drip. Since then the Cochrane collaborative has addressed the same question. They reviewed 5 trials including 201 total patients (some children). They found “low to very low-quality evidence that there are neither advantages nor disadvantages when comparing the effects of subcutaneous rapid-acting insulin analogues vs. IV regular insulin when treating mild to moderate DKA.” As long as the nurses are comfortable with q1 fingersticks, its something to consider next time you treat DKA. References Andrade-Castellanos CA, Colunga-Lozano LE, Delgado-Figueroa N, Gonzalez-Padilla DA. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. Cochrane Database of Systematic Reviews 2016, Issue 1. Art. No.: CD011281. D Continue reading >>

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