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Milwaukee Formula For Dka

Nuances In Resuscitation Part Iii: Diabetic Ketoacidosis

Nuances In Resuscitation Part Iii: Diabetic Ketoacidosis

Thus far we have discussed resuscitation in trauma and sepsis. What distinguishes those two from the resuscitation goals in DKA is timing. In trauma and sepsis, it’s all about early recognition, aggressive and quick optimization, and understanding all the possible treatment options at your disposal. In the management of DKA, it’s quite the opposite. If you remember anything from this discussion, it’s that slow and steady wins the race! In fact, overaggressive resuscitation is what leads to the most significant morbidity and mortality in DKA patients. Patients in DKA don’t die from the disease process – they die because we kill them! DKA is defined as an anion-gap metabolic acidosis, with elevated serum ketones (usually measured as beta-hydroxybutyrate), blood glucose > 250 mg/dL, pH < 7.3, and a serum HCO3 < 18 mEq/L. It is the reason for over 50% of diabetic admissions, and many DKA patients begin their inpatient hospital course in the ICU. The leading causes of DKA are medication non-compliance, underlying infection, new-onset diabetes (i.e. DKA is the first presenting illness), or underlying medical/surgical stress. In general, DKA patients will present to the ED relatively early in their disease process because the ketones produced by the body induce vomiting, prompting the patient to seek treatment. This is in contrast to hyperosmolar non-ketotic coma patients (HONK) that present much later in their illness because there are no ketones in the blood to induce vomiting and alert the patient or his/her family that something is wrong. The mainstays of DKA management are fluid replenishment, glycemic control, correction of any other metabolic anomalies, and treatment of any underlying cause for the glycemic derangement. There are definitely some differences in Continue reading >>

Pediatric Diabetic Ketoacidosistreatment & Management

Pediatric Diabetic Ketoacidosistreatment & Management

Pediatric Diabetic KetoacidosisTreatment & Management Author: William H Lamb, MD, MBBS, FRCP(Edin), FRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more... In patients with diabetic ketoacidosis, the first principals of resuscitation apply (ie, the ABCs [airway, breathing, circulation]). [ 3 ] Outcomes are best when children are closely monitored and a changing status is promptly addressed. [ 39 , 2 ] Give oxygen, although this has no effect on the respiratory drive of acidosis. Diagnose by clinical history, physical signs, and elevated blood glucose. Fluid, insulin, and electrolyte (potassium and, in select cases, bicarbonate) replacement is essential in the treatment of diabetic ketoacidosis. Early in the treatment of diabetic ketoacidosis, when blood glucose levels are very elevated, the child can continue to experience massive fluid losses and deteriorate. Strict measurement of fluid balance is essential for optimal treatment. Continuous subcutaneous insulin infusion therapy using an insulin pump should be stopped during the treatment of diabetic ketoacidosis. Children with severe acidosis (ie, pH < 7.1) or with altered consciousness should be admitted to a pediatric intensive care unit. In cases in which the occurrence of diabetic ketoacidosis signals a new diagnosis of diabetes, the process of education and support by the diabetes team should begin when the patient recovers. In cases in which diabetic ketoacidosis occurs in a child with established diabetes, explore the cause of the episode and take steps to prevent a recurrence. Following recovery from diabetic ketoacidosis, patients require subcutaneous insulin therapy. Edge JA, Roy Y, Bergomi A, et al. Conscious level in children with diabetic ketoacidosis is related to severity of acidosis and not to blood g Continue reading >>

Dka Paediatric

Dka Paediatric

4. Consider PICU or HDU for the following, and discuss with a paediatric consultant. severe acidosis pH<7.1 with marked hyperventilation sensorium with risk of aspiration from vomiting staffing levels on the wards are insufficient to allow adequate monitoring Where PICU or HDU do not exist within the admitting hospital, transfer to another hospital for such care (unless ventilatory support becomes necessary) may not be appropriate. However, ALL children with DKA are high-dependency patients and require a high level of nursing care, usually 1:1 even if on general paediatric wards. Ensure full instructions are given to the senior nursing staff emphasising the need for: strict fluid balance (urinary catheterisation may be required in young/sick children) measurement of volume of every urine sample hourly capillary blood glucose measurements (these may be inaccurate with severe dehydration/acidosis but useful in documenting the trends. Do not rely on any sudden changes but check with a venous laboratory glucose measurement) capillary blood ketone levels every 1-2 hours twice daily weight; can be helpful in assessing fluid balance hourly or more frequent neurological observations initially reporting immediately to the medical staff, even at night, symptoms of headache, or slowing of pulse rate, or any change in either conscious level or behaviour reporting any changes in the ECG trace, especially T wave changes suggesting hyper- or hypokalaemia Start recording all results and clinical signs on a flow chart. By this stage, the circulating volume should have been restored and the child no longer in shock. If not, give a further 10 ml/kg 0.9% saline (to a maximum of 30 ml/kg) over 30 minutes. (discuss with a consultant if the child has already received 30 ml/kg). Otherwise, on Continue reading >>

The Management Of Diabetic Ketoacidosis In Children

The Management Of Diabetic Ketoacidosis In Children

Go to: Abstract 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 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. Keywords: adolescents, cerebral edema, children, complications, diabetic ketoacidosis, fluid replacement, hypokalemia, management, prevention, recurrent DKA Go to: Introduction Definition of Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is biochemically defined as a venous pH <7.3 or serum Continue reading >>

Diabetic Ketoacidosis Including Fluid Calculation Sheet

Diabetic Ketoacidosis Including Fluid Calculation Sheet

Diabetic ketoacidosis including fluid calculation sheet Diabetic ketoacidosis including fluid calculation sheet Standardisation of the management of diabetic ketoacidosis in children, including an algorithm for intravenous fluid administration. Children with known or newly diagnosed diabetes mellitus. Medical and nursing staff that encounter this patient group. NB:There is no difference in the management of DKA in a new or established patient NB Urine output may remain fair because of osmotic diuresis NB These features usually present a few hours after commencing treatment but can occur very early 10ml plain tube for possible autoantibodies Glucose, Ketones (test all urine and record results) Measure current weight if at all possible Nil by mouth NG Tube if unconscious or evidence of gastric distention Repeat biochemistry frequently (~2hrly) until patient stable Fluids for DKA - use with DKA IV Fluid Calculation Sheet (below) Weigh the child and compare with previous known weights and centile charts - access the electronic medical record for existing patients. Treat shock with 10ml/kg N Saline. May repeat once before discussing with a consultant. Calculate fluid deficit - see A, B, C and D on calculation sheet Determine maintenance fluid volume per kg from age: (NB Maintenance calculation is for 48 hours) [48h MAINTENANCE (C x E) + DEFICIT (D x 1000)] - Volume used to treat shock Double check all calculations and have someone else do so independently - if you are in any doubt ASK Treat shock (resuscitate) with Normal Saline Sodium Bicarbonate is very rarely indicated and may be harmful - only consider in Intensive Care Unit after discussion with consultant - dose would be 0.5mmol/kg over 30 minutes Potassium can usually be added to bags immediately after resuscitation Continue reading >>

Dka: Management And Pitfalls

Dka: Management And Pitfalls

Published by Daniel Wickerham Modified over 3 years ago Presentation on theme: "DKA: Management and Pitfalls" Presentation transcript: Justin Bright, M.D. Emergency Physicians of NW Ohio February 20, 2013 2 Goals For Today Definitions and characteristics of DKA Appropriate workup Treatment modalities Identify pitfalls and complications Discuss difference in adult vs. pediatric population Management of DKA here at Henry Ford 3 What Is DKA? State of insulin deficiency (absolute or relative) causing dehydration, acidosis, and metabolic derangement By blood work Anion gap metabolic acidosis BHOB > 5 mEq/L Blood glucose > 250 mg/dL pH < 7.3 HCO3 < 18 mEq/L 4 The Stats DKA is reason for 50% of diabetic admissions Tends to occur in patients less than 19 yo Type 1 DM > Type 2 DM Death occurs in 2% of presenting patients 5 Causes of DKA? Underlying Infection (40%) Non-compliance with insulin regimen (25%) New onset diabetes (15%) Medical or surgical stress (20%) AMI Sepsis weak and dizzy Syncope Altered mental status 6 What Is Insulin? Anabolic regulatory hormone Released by pancreas (or administered as supplemental medication) in response to elevated blood sugar Causes blood sugar to be utilized for fuel, with excess stored as muscle and fat Inhibits release of glucagon Inhibits gluconeogenesis and glycogenolysis Hepatic gluconeogenesis and glycogenolysis Fatty acid break down ketogenesis Byproducts: ketones (acetone, BHOB, acetoacetate) Excess blood glucose osmotic diuresis BHOB induces vomiting more dehydration Rising acidosis potassium shift and osmotic loss 9 What Does DKA Look Like? Insidious onset Weakness, fatigue, malaise Polydypsia, polyuria Weakness, fatigue, malaise Abdominal pain and vomiting as BOHB increases Altered level of consciousness May present with symptom Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

DKA is the end result of the metabolic abnormalities resulting from a severe deficiency of insulin or insulin effectiveness. Deficiency of insulin effectiveness occurs during stress as counter-regulatory hormones block insulin action. DKA occurs in 20-40% of children with new-onset diabetes, and in children with known diabetes who omit insulin doses or who do not successfully manage an intercurrent illness. DKA is typically characterized by: Hyperglycemia over 300 mg/dl. Low bicarbonate (<15 mEq/L). Acidosis (pH <7.30). Polyuria, polydipsia, fatigue, headache, dry mouth, nausea, abdominal pain, and vomiting. Lethargy , obtundation and coma. Include tachycardia and deep heavy rapid breathing (Kussmaul's respirations). Diffuse abdominal tenderness, with negative rebound. Electrolytes with calculated anion gap and effective osmolality Beta-hydroxybutyrate or serum ketones if not available Complete urinalysis with urine ketones by dipstick As indicated cultures of urine, blood, throat, or other sites of suspected infection Chest radiography if pneumonia or cardiopulmonary disease is suspected The Milwaukee protocol has been used for more than 20 yr in a large clinic setting with no deaths and no neurologic sequelae in any child treated with this protocol. It can be used for children of all ages and with all degrees of DKA. It is designed to restore most electrolyte deficits, to reverse the acidosis, and to rehydrate the moderately ill child in about 24 hr. A standard water deficit (85 mL/kg) is assumed. Children with milder DKA recover in 10 to 20 hr, whereas those with more severe DKA require 30 to 36 hr with this protocol. Insulin infusion is begun at a rate of 0.1 unit/kg/h and must be continued till the correction of acidosis. Glucose usually as 5% solution must be add Continue reading >>

University Of Zagreb

University Of Zagreb

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

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