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Diabetic Ketoacidosis Treatment Guidelines

Diagnosis

Diagnosis

Print If your doctor suspects diabetic ketoacidosis, he or she will do a physical exam and various blood tests. In some cases, additional tests may be needed to help determine what triggered the diabetic ketoacidosis. Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: Blood sugar level. If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar level will continue to rise. Ketone level. When your body breaks down fat and protein for energy, acids known as ketones enter your bloodstream. Blood acidity. If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the normal function of organs throughout your body. Additional tests Your doctor may order tests to identify underlying health problems that might have contributed to diabetic ketoacidosis and to check for complications. Tests might include: Blood electrolyte tests Urinalysis Chest X-ray A recording of the electrical activity of the heart (electrocardiogram) Treatment If you're diagnosed with diabetic ketoacidosis, you might be treated in the emergency room or admitted to the hospital. Treatment usually involves: Fluid replacement. You'll receive fluids — either by mouth or through a vein (intravenously) — until you're rehydrated. The fluids will replace those you've lost through excessive urination, as well as help dilute the excess sugar in your blood. Electrolyte replacement. Electrolytes are minerals in your blood that carry an electric charge, such as sodium, potassium and chloride. The absence of insulin can lower the level of several electrolytes in your blood. You'll receive electrolytes throu Continue reading >>

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc 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 >>

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

Diabetic Ketoacidosis

Authors Runa Acharya, MD, University of Iowa-Des Moines Internal Medicine Residency Program at UnityPoint Health, Des Moines, IA Udaya M. Kabadi, MD, FACP, FRCP(C), FACE, Veteran Affairs Medical Center and Broadlawns Medical Center, Des Moines, IA; Des Moines University of Osteopathic Medicine, Iowa City; and University of Iowa Carver College of Medicine, Iowa City; Adjunct Professor of Medicine and Endocrinology, University of Iowa, Iowa City, and Des Moines University, Des Moines Peer Reviewer Jay Shubrook, DO, FAAFP, FACOFP, Professor, Primary Care Department, Touro University, College of Osteopathic Medicine, Vallejo, CA Statement of Financial Disclosure To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, Dr. Kabadi (author) reports he is a consultant and on the speakers bureau for Sanofi. Dr. Shubrook (peer reviewer) reports he receives grant/research support from Sanofi and is a consultant for Eil Lilly, Novo Nordisk, and Astra Zeneca. Dr. Acharya (author) reports no financial relationships relevant to this field of study. Continue reading >>

Fluid Replacement Give Sodium Chloride 0.9% Intravenously As Follows:

Fluid Replacement Give Sodium Chloride 0.9% Intravenously As Follows:

Diabetic emergencies: guidelines for the management of diabetic ketoacidosis and management of hyperosmolar non-ketotic diabetic coma The following guideline is approved only for use at University College London Hospitals NHS Foundation Trust. It is provided as supporting information for the UCLH Injectable Medicines Administration Guide. Neither UCLH nor Wiley accept liability for errors or omissions within the guideline. Wherever possible, users of the Guide should refer to locally produced practice guidelines. UCLH’s guidelines represent the expert opinion of the clinicians within the hospital and may not be applicable to patients outside the Trust. Adapted from UCLH Guidelines for the management of common medical emergencies and for the use of antimicrobial drugs Reviewed by: Dr Stephanie Baldeweg, Consultant Endocrinologist, UCLH and Mrs Sejal Rabone, Pharmacist, MES Directorate, UCLH January 2006 Management of diabetic ketoacidosis and management of hyperosmolar The principal problems are dehydration and acidosis. Diabetic ketoacidosis is a medical emergency. Aim of treatment: Correct acidosis with IV fluids and insulin, and restore electrolyte balance. Criteria for diagnosis: • Blood glucose > 10 mmol/L and • Positive urine ketones test and • Acidosis (pH ≤ 7.3 or bicarbonate ≤ 15 mmol/L) Also look for thirst and polyuria, hyperventilation (Kussmaul), abdominal pain, vomiting. Immediate admission to critical care must take priority over all except lifesaving interventions. Refer the patient to the DMR immediately whilst continuing management in A&E. Contact a member of the diabetic team (registrar bleep MX109); it is better to seek advice early than late. Urgent Investigations • Blood glucose. This is accurate up to abou Continue reading >>

Type 1 Diabetes In Adults: Diagnosis And Management

Type 1 Diabetes In Adults: Diagnosis And Management

High blood glucose (hyperglycaemia) that is not treated can lead to a serious condition called diabetic ketoacidosis (or DKA for short). It is caused by the build‑up of harmful ketones in the blood. People with type 1 diabetes are at risk of DKA. You may be advised to test for ketones in your blood or urine as part of sick-day rules. Your blood ketones may be measured by a healthcare professional if it is thought you might have DKA. If you have DKA you will need emergency treatment in hospital by a specialist care team. This will include having fluids through a drip. Questions to ask about DKA 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 >>

Diabetes Mellitus

Diabetes Mellitus

See also: 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 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' below). Assessment of children and adolescents with DKA 1. Degree Of Dehydration (often over-estimated) None/Mild ( < 4%): no clinical signs Moderate (4-7%): easily detectable dehydration eg. reduced skin turgor, poor capillary return Severe(>7%): poor perfusion, rapid pulse, reduced blood pressure i.e. shock 3. Investigations Venous blood sample (place an i.v. line if possible as this will be needed if DKA is confirmed) for the following: FBE Blood glucose, urea, electrolytes (sodium, potassium, calcium, magnesium, phosphate) Blood ketones (bedside test) Venous blood gas (including bicarbonate) Investigations for precipitating cause: if clinical signs of infection consider septic work up including blood culture For all newly diagnosed patients: Insulin antibodies, GAD antibodies, coeliac screen (total IgA, anti-gliadin Ab, tissue transglutaminase Ab) and thyroid function 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 >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i 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 >>

Diagnosis And Treatment Of Diabetic Ketoacidosis

Diagnosis And Treatment Of Diabetic Ketoacidosis

85 Abstract Diabetic ketoacidosis (DKA) is the most frequent hyperglycaemic acute diabetic complication. Furthermore it carries a significant risk of death, which can be prevented by early and effective management. All physicians, irrespective of the discipline they are working in and whether in primary, secondary or tertiary care institutions, should be able to recognise DKA early and initiate management immediately. 86 Introduction Diabetic ketoacidosis (DKA) is a common complication of diabetes with an annual occurrence rate of 46 to 50 per 10 000 diabetic patients. The severity of this acute diabetic complication can be appreciated from the high death-to-case ratio of 5 to 10%.1 In Africa the mortality of DKA is unacceptably high with a reported death rate of 26 to 29% in studies from Kenya, Tanzania and Ghana.2 It is a complication of both type 1 and type 2 diabetes mellitus, although more commonly seen in type 1 diabetic patients. Of known diabetic patients presenting with DKA about one-quarter will be patients with type 2 diabetes. In patients presenting with a DKA as first manifestation of diabetes about 15% will be type 2.3 This correlates well with data from South Africa suggesting that one- quarter of patients with DKA will be type 2 with adequate C-peptide levels and the absence of anti-GAD antibodies.4 This review will focus on the principles of diagnosis, monitoring and treatment of DKA, with special mention of new developments and controversial issues. Clinical features DKA evolves over hours to days in both type 1 and type 2 diabetic patients, but the symptoms of poor control of blood glucose are usually present for several days before the onset or presentation of ketoacidosis.5 The clinical features of DKA are non-specific and patients may present with 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 >>

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 >>

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