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What Is Dka Protocol?

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 (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Also known as: DKA Severe diabetic ketoacidosis is a medical emergency and requires prompt treatment to correct dehydration, electrolyte disturbances and acidosis. It is a complication of insulin dependent Diabetes Mellitus. DKA is the result of marked insulin deficiency, and ketonaemia and ketoacidosis occur approximately 15 days after insulin concentrations are suppressed to fasting levels. Marked insulin suppression occurs on average 4 days after fasting glucose levels reach 30mmol/L. Many cats with DKA have other intercurrent conditions which may precipitate the condition including: infection, pancreatitis or renal insufficiency. Pathophysiology Insulin deficiency leads to increased breakdown of fat that releases fatty acids into the circulation. Free fatty acids are oxidised in the liver to ketones that are used by many tissues as an energy source instead of glucose. This occurs when intracellular levels of glucose are insufficient for energy metabolism as a result of severe insulin deficiency. In the liver, instead of being converted to triglycerides, free fatty acids are oxidised to acetoacetate, which is converted to hydroxybutyrate or acetone. Ketones are acids that cause central nervous system depression and act in the chemoreceptor trigger zone to cause nausea, vomiting and anorexia. They also accelerate osmotic water loss in the urine. Dehydration results from inadequate fluid intake in the face of accelerated water loss due to glucosuria and ketonuria. Dehydration and subsequent reduced tissue perfusion compounds the acidosis through lactic acid production. There is whole body loss of electrolytes including sodium, potassium, magnesium and phosphate and there is also intracellular redistribution of electrolytes following insulin therapy which may compound p Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Treatment Of Diabetic Ketoacidosis With Subcutaneous Insulin Aspart

Treatment Of Diabetic Ketoacidosis With Subcutaneous Insulin Aspart

Abstract OBJECTIVE—In this prospective, randomized, open trial, we compared the efficacy and safety of aspart insulin given subcutaneously at different time intervals to a standard low-dose intravenous (IV) infusion protocol of regular insulin in patients with uncomplicated diabetic ketoacidosis (DKA). RESEARCH DESIGN AND METHODS—A total of 45 consecutive patients admitted with DKA were randomly assigned to receive subcutaneous (SC) aspart insulin every hour (SC-1h, n = 15) or every 2 h (SC-2h, n = 15) or to receive IV infusion of regular insulin (n = 15). Response to medical therapy was evaluated by assessing the duration of treatment until resolution of hyperglycemia and ketoacidosis. Additional end points included total length of hospitalization, amount of insulin administration until resolution of hyperglycemia and ketoacidosis, and number of hypoglycemic events. RESULTS—Admission biochemical parameters in patients treated with SC-1h (glucose: 44 ± 21 mmol/l [means ± SD], bicarbonate: 7.1 ± 3 mmol/l, pH: 7.14 ± 0.09) were similar to those treated with SC-2h (glucose: 42 ± 21 mmol/l, bicarbonate: 7.6 ± 4 mmol/l, pH: 7.15 ± 0.12) and IV regular insulin (glucose: 40 ± 13 mmol/l, bicarbonate 7.1 ± 4 mmol/l, pH: 7.11 ± 0.17). There were no statistical differences in the mean duration of treatment until correction of hyperglycemia (6.9 ± 4, 6.1 ± 4, and 7.1 ± 5 h) or until resolution of ketoacidosis (10 ± 3, 10.7 ± 3, and 11 ± 3 h) among patients treated with SC-1h and SC-2h or with IV insulin, respectively (NS). There was no mortality and no differences in the length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or the number of hypoglycemic events among treatment groups. CONCLUSIONS—Ou Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Protocols And Order Sets

Protocols And Order Sets

The order sets provided here are only a few examples from institutions involved in the management of inpatient hyperglycemia; this is not an all-inclusive list. Posting of these protocols does not constitute endorsement of any specific protocol. We believe that each institution should consult with diabetes experts to select and implement insulin protocols. Key Points Successful implementation of protocols requires: Buy-in from key stakeholders (critical care physicians, house staff, nursing, pharmacy, hospital administration, etc) Appropriate education through in-servicing of hospital staff Ongoing monitoring of results Support from endocrinologists for specific questions or when a patient does not respond to the protocol as expected It is important to keep in mind that these algorithms have not been directly compared in clinical trials. In selecting a protocol, one should look for characteristics that are compatible with the institution in which it will be implemented. Consideration should be given to the following characteristics and whether these attributes will fit within the institution: Is the protocol dynamic (ie, does it allow for variability in insulin requirements and account for rates of change in blood glucose concentrations)? What is its relative user-friendliness and complexity? To what extent does it require performance of basic calculations? Is it compatible with the local computer systems? None of the examples provided are suitable for the treatment of diabetic ketoacidosis. 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 >>

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 >>

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 >>

1. Initiate Iv Fluids Stat: Ivf Should Be Started In The Ed And Continued In Icu As Needed

1. Initiate Iv Fluids Stat: Ivf Should Be Started In The Ed And Continued In Icu As Needed

· Estimate intravascular volume status (via BUN/Cr, VS, orthostatic BP, urine output, physical exam, HgB)(to estimate saline requirement. · Assess free water deficit using corrected serum Na. A. Initial Fluid Orders: I. First correct intravascular fluid volume deficit with normal saline at a rate dependant on severity (being more cautious if cardiac or renal disease) a) 0.9% NaCl at 1-3 Liters /hr (15-20ml/kg) over 1 hour b) Give additional 0.9% NaCl IV rapidly if patient remains volume depleted. B. While Blood Glucose greater than 250 mg/dL -- Subsequent Fluid Orders: I. Calculate corrected Na: a) Corrected Sodium less than 134 mEq/L: continue 0.9% NaCl IV at 250-500 ml/hr until glucose less than 250 mg/dL, or corrected Na greater than 134 mEq/L. b) Corrected Sodium greater than or equal to 134 mEq/L: continue with 0.45% NaCl IV at 250-500 ml/hour until glucose less than 250 mg/dL, or corrected Na less than 134 mEq/L. II. If corrected Na decreases more than 2 mEq per hour, consider slowing the infusion rate. C. WHEN Blood Glucose less than 250mg/dL -- Subsequent Fluid Orders: I. Calculate corrected Na: a) Corrected sodium less than134 mEq/L: D5W/0.9% NaCl IV at 100 - 200 ml/hr b) Corrected Sodium greater than or equal to 134 mEq/L: D5W/0.45% NaCl IV at 100 - 200 ml/hr 2. Insulin Administration: · Hold all home anti-diabetic medications. · Initiate Insulin therapy AFTER IV fluid resuscitation has begun (500 ml or greater) and when potassium is 3.2 mEq/L or greater. · Insulin Infusion starting dose: (See Step 1 in Insulin Infusion Protocol; Page 4) A. Blood Glucose greater than or equal to 300mg/dL ( give 0.1 units/kg IV bolus and begin insulin infusion at 0.1 units/kg/hour, rounded to 0.5 unit increment, and use Insulin Infusion Protocol. B. Blood Glucose Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Diabetic Ketoacidosis In Dogs

Diabetic Ketoacidosis In Dogs

My dog is diabetic. He has been doing pretty well overall, but recently he became really ill. He stopped eating well, started drinking lots of water, and got really weak. His veterinarian said that he had a condition called “ketoacidosis,” and he had to spend several days in the hospital. I’m not sure I understand this disorder. Diabetic ketoacidosis is a medical emergency that occurs when there is not enough insulin in the body to control blood sugar (glucose) levels. The body can’t use glucose properly without insulin, so blood glucose levels get very high, and the body creates ketone bodies as an emergency fuel source. When these are broken down, it creates byproducts that cause the body’s acid/base balance to shift, and the body becomes more acidic (acidosis), and it can’t maintain appropriate fluid balance. The electrolyte (mineral) balance becomes disrupted which can lead to abnormal heart rhythms and abnormal muscle function. If left untreated, diabetic ketoacidosis is fatal. How could this disorder have happened? If a diabetic dog undergoes a stress event of some kind, the body secretes stress hormones that interfere with appropriate insulin activity. Examples of stress events that can lead to diabetic ketoacidosis include infection, inflammation, and heart disease. What are the signs of diabetic ketoacidosis? The signs of diabetic ketoacidosis include: Excessive thirst/drinking Increased urination Lethargy Weakness Vomiting Increased respiratory rate Decreased appetite Weight loss (unplanned) with muscle wasting Dehydration Unkempt haircoat These same clinical signs can occur with other medical conditions, so it is important for your veterinarian to perform appropriate diagnostic tests to determine if diabetic ketoacidosis in truly the issue at hand 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 >>

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