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Dka Guidelines

Management Of Diabetic Ketoacidosis (dka)

Management Of Diabetic Ketoacidosis (dka)

Management of Acute Diabetic Ketoacidosis (DKA) Below is the link to the care pathway for the management of diabetic ketoacidosis in adults. Specific guidelines exist for the management of DKA in children. In patients aged 13-16 years presenting with DKA, the management of DKA should be discussed with relevant paediatric staff. Diagnosis Severe uncontrolled diabetes with: Hyperglycaemia (blood glucose >14mmol/L, usually but not exclusively) Metabolic acidosis (H+ >45mEq/L or HCO3- <18mmol/L or pH <7.3 on venous gases) Ketonaemia (>3mmol/L) / ketonuria (>++) Severity criteria One or more of the following may indicate severe DKA and should be considered for level 2 care (MHDU if available). It may also be necessary to consider a surgical cause for the deterioration. Blood ketones >6mmol/L Bicarbonate level <5mmol/L Venous / artierial pH <7.1 Hypokalaemia on admission (<3.5mmol/L) GCS <12 or abnormal AVPU scale Oxygen saturation <92% on air (assuming normal baseline respiratory function) Systolic BP <90mmHg, pulse >100bpm or <60bpm Anion gap >16 [anion gap = (Na+ + K+) – (Cl- + HCO3-)] Cerebral oedema The care pathways for the emergency management of DKA should be used for all eligible patients. Complete pathways for 0–4 hours and 4 hours–discharge for each DKA episode. These provide instruction on fluid balance, insulin and potassium replacement. Please note there are DKA order sets on TrakCare (DKA baseline and DKA continuing care). The care pathways are available within relevant departments or online at NHSGGC Managed Clinical Networks / Diabetes MCN / Clinical Guidelines and Protocols / DKA Care Pathway. Supplementary notes as per care pathway 0–4 hours Continue background SC insulin (glargine, levemir, degludec, isophane insulin) while on fixed rate intravenou Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

Diagnosis And Management Of Hyperglycemic Crises: Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Management Of Hyperglycemic Crises: Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Download Slide Library Key Points DKA and HHS are life-threatening emergencies. Management involves Attention to precipitating cause Fluid and electrolyte management Insulin therapy Patient monitoring Prevention of metabolic complications during recovery Transition to long-term therapy Patient education and discharge planning should aim at prevention of recurrence. Suggested Reading Burghen GA, Etteldorf JN, Fisher JN, Kitabchi AQ. Comparison of high-dose and low-dose insulin by continuous intravenous infusion in the treatment of diabetic ketoacidosis in children. Diabetes Care. 1980;3:15-20. Devi R, Selvakumar G, Clark L, Downer C, Braithwaite SS. A dose-defining insulin algorithm for attainment and maintenance of glycemic targets during therapy of hyperglycemic crises. Diabetes Manage. 2011;1:397-412. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344:264-269. Mudaliar S, Mohideen P, Deutsch R, et al. Intravenous glargine and regular insulin have similar effects on endogenous glucose output and peripheral activation/deactivation kinetic profiles. Diabetes Care. 2002;25:1597-1602. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care. 2004;27:1541-1546. Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

Pediatric Diabetic Ketoacidosis – Guideline From Royal Children’s Hospital Melbourne

Pediatric Diabetic Ketoacidosis – Guideline From Royal Children’s Hospital Melbourne

Our goal as primary care physicians is to make the diagnosis of Type 1 Diabetes or Diabetic Ketoacidosis at the earliest opportunity and then immediately arrange for inpatient expert follow up at a tertiary care center. Twenty-five percent of patients with a new diagnosis of diabetes present with diabetic ketoacidosis; a missed diagnosis of diabetes is the most common cause, especially in young children. [from Pediatric Diabetic Ketoacidosis Emergency Department Care of emedicine.medscape.com] What follows are excerpts of Pediatric Type 1 Diabetes Mellitus Clinical Presentation Updated: Apr 27, 2017 from emedicine.medscape.com: Symptoms of ketoacidosis These symptoms include the following: What follows are only excerpts from the Diabetes Mellitus Guideline. Please see the complete protocol] on diabetic ketoacidosis from the Royal Children’s Hospital Melbourne: Background: Diabetic ketoacidosis (DKA) is the combination of hyperglycemia, metabolic acidosis, and ketonaemia. It may be the first presentation for a child with previously undiagnosed diabetes. It can also be precipitated by illness, or poor compliance with taking insulin. All patients presenting with a blood glucose level (BGL) ≥ 11.1mmol/l [200 mg/dl] should have blood ketones tested on a capillary sample using a bedside OptiumTM meter. If this test is positive (>0.6 mmol/l), assess for acidosis to determine further management. Urinalysis can be used for initial assessment if blood ketone testing is not available. The biochemical criteria for DKA are: 1. Venous pH < 7.3 or bicarbonate <15 mmol/l 2. Presence of blood or urinary ketones If ketones are negative, or the pH is normal in the presence of ketones, patients can be managed with subcutaneous (s.c.) insulin (see ‘ new presentation, mildly ill‘ bel Continue reading >>

Updated Feb 2017 J Clayton

Updated Feb 2017 J Clayton

NUH Management of Diabetic Ketoacidosis in Adults (18 years old & over) (Please see the Paediatric guidelines for patients under 18 years) If in doubt, call someone more senior. KETOACIDOSIS CAN KILL. Use in conjunction with the NUH pathway of care for DKA in adults (insulin prescription, administration and monitoring chart). 1. DIAGNOSIS All three required 1. Raised blood glucose>11mmol /L or known diabetes 2. Capillary ketones > 3 mmol/L (or Ketones >2+ in urine) 3. Venous pH < 7.35 or venous bicarb < 15mmol/L 2. ESSENTIAL INVESTIGATIONS Arterial puncture NOT routinely needed  U+E, creatinine, blood glucose  Venous blood gas for bicarbonate, potassium and pH (analyse on machine on B3, ED, HDU, ITU)  ECG/CXR/MSU/blood cultures/pregnancy test depending on clinical suspicion Raised WCC and serum amylase are common in DKA and do not usually suggest pancreatitis. 4. IMMEDIATE TREATMENT START IN EMERGENCY DEPT / ASSESSMENT UNIT OR THEIR CURRENT LOCATION. DELAY IN STARTING TREATMENT MAY BE FATAL. 1. Insert venflon 2. 1L 0.9% sodium chloride infusion over 1hr if systolic BP>90 (If systolic BP<90 give repeated boluses of 500ml 0.9% sodium chloride over 10-15 minutes) 3. Start IV insulin infusion: 50 units human soluble (ACTRAPID®) insulin added to 49.5 mls 0.9% sodium chloride to give a 1 unit/ml solution via syringe driver at 0.1 units/ kg / hr (estimated or actual weight) 3. SEVERITY (Venous bicarbonate or pH) >14 mmol/l or pH >7.3 Mild 10-14 mmol/l or pH 7.1-7.3 Moderate < 10 mmol/l or pH <7.1 Severe 5. TRANSFER NO PATIENT WITH DKA SHOULD BE TRANSFERRED BETWEEN HOSPITALS URGENT CRITICAL CARE/HDU REVIEW if any of: Venous bicarbonate < 10 mmol/l or pH<7.1, drowsy (P or U on AVPU), fluid balance problems, pregnancy, co morbidities, sats<94% on 40% O2, p Continue reading >>

Ispad Clinical Practice Consensus Guidelines 2014

Ispad Clinical Practice Consensus Guidelines 2014

Editor in Chief: Mark A. Sperling, Pittsburgh, USA. Guest Editors: Carlo Acerini, Maria E Craig, Carine de Beaufort, David M Maahs and Ragnar Hanas. Introduction Carlo Acerini, Maria E Craig, Carine de Beaufort, David M Maahs and Ragnar Hanas. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 1–3. Uploaded: 2. Sept 2014 Download Introduction Chapter 1: Definition, epidemiology, diagnosis and classification Craig ME, Jefferies C, Dabelea D, Balde N, Seth A, Donaghue KC. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 4–17. Uploaded: 2. Sept 2014 Download Chapter 1 Chapter 2: Phases of Type 1 Diabetes Couper JJ, Haller MJ, Ziegler A-G, KnipM, Ludvigsson J, Craig ME. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 18–25. Download Chapter 2 Chapter 3: Type 2 diabetes Zeitler P, Fu J, Tandon N, Nadeau K, Urakami T, Bartlett T, Maahs D. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 26-46. Uploaded: 2. Sept 2014 Download Chapter 3 Chapter 4: The Diagnosis and Management of Monogenic diabetes Rubio-Cabezas O, Hattersley AT, Njølstad PR, Mlynarski W, Ellard S,White N, Chi DV, Craig ME. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 47-64. Uploaded: 2. Sept 2014 Download Chapter 4 Chapter 5: Management of cystic fibrosis-related diabetes Moran A, Pillay K, Becker DJ, Acerini CL. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 65-76. Uploaded: 2. Sept 2014 Download Chapter 5 Chapter 6: Diabetes education Lange K, Swift P, Pankowska E, Danne T. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 77-85. Uploaded: 2. Sept 2014 Download Chapter 6 Chapter 7: The delivery of ambulatory diabetes care Pihoker C, Forsander G, Fantahun B, Virmani A, Luo X, Hallman M, Wolfsdorf J, Maahs DM. Published in Pediatric Diabetes 2014: 15(Suppl. 20): 86-101. Up Continue reading >>

Diabetic Ketoacidosis (dka): Treatment Guidelines

Diabetic Ketoacidosis (dka): Treatment Guidelines

Diabetic ketoacidosis (DKA), resulting from severe insulin deficiency, accounts for most hospitalization and is the most common cause of death, mostly due to cerebral edema, in pediatric diabetes. This article provides guidelines on management to restore perfusion, stop ongoing ketogenesis, correct electrolyte losses, and avoid hypokalemia and hypoglycemia and the circumstances that may contribute, in some instances, to cerebral edema (overhydration, rapid osmolar shifts, hypoxia). These guidelines emphasize the importance of monitoring glycemia, electrolytes, hydration, vital signs, and neurologic status in a setting where response can be rapid if necessary (e.g., mannitol for cerebral edema). Most important is the prevention of DKA in established patients by close supervision of those most likely to omit insulin, or during illness, and a high index of suspicion for diabetes to prevent deterioration to DKA in new patients, particularly those under age 5, who are at greatest risk of complications. Continue reading >>

Management Of Paediatric Diabetic Ketoacidosis: An Audit

Management Of Paediatric Diabetic Ketoacidosis: An Audit

Introduction: NICE Guidelines NG18 (published 2015) advocate a more conservative approach to management of diabetic ketoacidosis (DKA) in children and young people up to the age of 18, in an attempt to reduce the risk of cerebral oedema. We aimed to assess if management of DKA in children at Manor Hospital was compliant with hospital guidelines, that were based on BSPED guidelines (issued 2009). We analysed the difference in total fluid administered if the new DKA guidelines were in place, specifically in the case of young people. Method: We retrospectively audited case notes of all patients up to the age of 19 years admitted to Walsall Manor Hospital with DKA between 1st July 2014–31st July 2015 (n=13). A standardised proforma was used to collect data, which was then analysed. Results: Current hospital policy advocates that young people after their 16th birthday are managed by the adult medical team. The adult DKA Guideline is based on recommendations of Joint British Diabetes Societies Inpatient Care Group recommendations (2013). The age range was 10 to 18 years. Ten patients were treated using the paediatric and three were treated using the adult guidelines. There was one significant fluid calculation error found in a patient treated with the paediatric guidelines, although the patient did not come to any harm. No fluid calculation error was found in those patients treated with adult guidelines, though one patient developed fluid overload not requiring active treatment. Mathematical modelling of fluid given in the first 12 hours of treatment shows that a young person would receive 40–70% less fluids if treated as per NICE NG18 instead of adult DKA Guidelines. In terms of other complications, there were 12 episodes of hypoglycaemia, but no episodes of hypokalaemia Continue reading >>

Management Of Diabetic Ketoacidosis In Adults

Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis is a potentially life-threatening complication of diabetes, making it a medical emergency. Nurses need to know how to identify and manage it and how to maintain electrolyte balance Continue reading >>

(pdf) Diabetic Ketoacidosis (dka): Treatment Guidelines

(pdf) Diabetic Ketoacidosis (dka): Treatment Guidelines

The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral ... [Show full abstract] edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%-70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 1-2 hours; an initial bolus of 10-20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%-10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort. This review deals with the two most serious side effects encountered with insulin pump therapy, severe hypoglycemia and diabetic ketoacidosis (DKA). Although clinical follow-up studies reported decreased rates of severe hypoglycemia, randomized studies have not confirmed this, showing no diff Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

DIABETIC KETOACIDOSIS AND THE HYPERGLYCEMIC hyperosmolar state are the most serious complications of diabetic decompensation and remain associated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ketoacidosis and electrolyte deficits. Diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS) appear as 2 extremes in the spectrum of diabetic decompensation.1 They remain the most serious acute metabolic complications of diabetes mellitus and are still associated with excess mortality. Because the approach to the diagnosis and treatment of these hyperglycemic crises are similar, we have opted to address them together. The incidence of DKA is between 4.6 and 8.0 per 1000 person-years among patients with diabetes, whereas that of HHS is less than 1 per 1000 person-years.2 Based on the estimated diabetic population in Canada,3 we can anticipate that 5000–10 000 patients will be admitted to hospital because of DKA every year and 500–1000 patients because of HHS. The estimated mortality rate for DKA is between 4% and 10%, whereas the rate for HHS varies from 10% to 50%, the rang 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 >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

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