Diabetic Ketoacidosis Clinical Practice Guidelines Order BMP, VBG, UA Check neuro status Consider New onset labs* Patient arrives with DKA Rehydration with normal saline 20ml/kg Signs of uncompensated shock after first bolus? No Check neuro status TIVF at 1.5-2.0x MIVF via 2 bag method*(below) Glucose infusion rate determined by the patient’s blood sugar (see chart on pg2) Insulin infusion at 0.1 units/kg/hr BMP q4h and start Insulin infusion at 0.1 units/kg/hr (for most patients). pH > 7.0 with trend of patient improvement? Obtain VBG q1h until upward trend is established AND pH > 7.0 Yes Yes No Repeat fluid bolus Continue rehydration with 1.5-2.0x MIVF by 2 bag method* without additional potassium Recheck potassium in no more than 4 hours Continue IVF at 1.5-2.0 x MIVF with NS as the base solution for the 2 bag method* with potassium as indicated until sodium is corrected and neuro status is baseline. No K< 5.0? Yes Continue rehydration with 2 bag method*; add a total of 40 mEq/L of K+ to IV fluids (as KCL 20mEq/L and KPO 20 mEq/L) Continue q1h glucose checks & rehydration for 8-12hrs of total fluids No Normal sodium & baseline neuro status? Yes Transition base IVF to ½ NS solution with standard 2 bag method BMP every 8 hrs until corrected PO sugar free Bicarb 18 or greater? Bicarb ≥ 16 x 2 with gap <10? Yes No Diabetic Ketoacidosis or DKA is a condition that occurs when there are critically low levels of insulin in the body. The body responds by burning fatty acids (ketogenesis) which produce acetone and betahydroxybutyric acid in very large amounts (acidosis) resulting in extreme dehydration, kidney failure, cardio-respiratory collapse and death if not treated. General Information This pathway is intended to treat mild to moderate uncomplicated DKA (pH > 7.0). Symptomatic Cerebral Edema from DKA is a clinical emergency. Warnings and emergency therapies Pediatric DKA is associated with a higher incidence of cerebral edema and stroke For concern of cerebral edema, consider hypertonic saline administration: 3-5ml/kg over 10 minutes (max of 500ml). Bicarbonate administration is associated with increased morbidity/mortality from cerebral edema. Infection can adversely affect the recovery time from DKA and threaten the clinical stability of the patient. When fever of > 100 F is present , the work up should include a fever/ infection evaluation while treating DKA *2 Bag Method The first bag is non-dextrose fluid and the second bag is D10; Both will be infused simultaneously via IV. Each bag will infuse at different rates dependent on serum glucose levels . Bicarbonate administration should be reserved for dire situations after consultation with a Pediatric Endocrinologist (information for glucose infusion w/ table on pg 2) Transition as follows: Allow patient to eat regular diet Give scheduled SQ insulin Stop insulin and dextrose fluids 10 min after SQ insulin Inclusion Criteria Patient must meet all of the following: Blood glucose > 250 Ketosis by blood or urine testing Acidosis by blood gas analysis AND any of the three listed below: History of previously diagnosed IDDM History of significant NIDDM History consistent with new onset IDDM (polyuria, polydipsia, polyphagia) Exclusion Criteria Significant dehydration/ketosis without insulin deficiency from any other cause, such as: Appendicitis or other abdominal crisis Steroid induced hyperglycemia Ketosis from other metabolic/genetic causes This guideline does not take into account individual patient situations, and does not substitute for clinical judgment Diabetic Ketoacidosis Clinical Practice Guidelines Insulin Infusion After initiation of insulin infusion: Bedside glucose testing hourly. Obtain BMP 4 hours for the first 8-12 hours of rehydration therapy. Consult Endocrinology for long acting insulin (Lantus) recommendations during rehydration. If the patient returns to baseline neurologic status and does not have documented hyponatremia (corrected for serum glucose), sugar-free clears up to 1 ml/kg/hr are allowed keeping total intake less than 2.5x MIVF. After 8-12 hours of rehydration therapy: Obtain new BMP. Provider team will assess patient for return to baseline neuro status, signs of cerebral edema, and correction of hyponatremia (>135 mEq/L) Continue rehydration per algorithm. Obtain BMP every 8 hours until acidosis is corrected. Transition from Insulin Infusion Obtain pre-meal glucose level by finger stick. Give patient the scheduled subcutaneous insulin injection including. sliding scale and/ or meal correction dose. Allow patient to eat 10 minutes after injection of meal insulin. Stop insulin infusion 20 minutes after meal insulin injection. If dehydration is still problematic, the pediatric endocrinology team will decide on IV fluids type, infusion rate and glucose infusion rate. Glucose Infusion Glucose infusion rate is determined by the patient’s blood sugar while on an insulin infusion as listed in the table below. The purpose of glucose in intravenous fluids is to provide enough dextrose to maintain the insulin infusion at all times in order to stop the catabolic process (ketogenesis). 1st Bag Patient’s Glucose (D0 solution) 2nd Bag (D10 solution) BG <200 0% TIVF (0x MIVF) 100% TIVF (1.5-2.0x MIVF) BG 201-300 50% TIVF (0.75-1.5x MIVF) 50% TIVF (0.75-1.5x MIVF) BG >301 100% TIVF (1.5-2.0x MIVF) 0% TIVF (0x MIVF) Patient Education Patient education is performed by both the bedside staff and the diabetes education nurse/endocrinology team. The provider places an order to page the diabetic educator (during regular week day work hours) for the standardized education pathway and approved education materials. REFERENCES Dunger, D. B., Sperling, M. A., Acerini, C. L., Bohn, D. J., Daneman, D., Danne, T. P. A., … Lawson Wilkins Pediatric Endocrine Society. (2004). European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society consensus statement on diabetic ketoacidosis in children and adolescents. Pediatrics, 113(2), e133–140. Felner, E. I., & White, P. C. (2001). Improving management of diabetic ketoacidosis in children. Pediatrics, 108(3), 735– 740. Fiordalisi, I., Novotny, W. E., Holbert, D., Finberg, L., Harris, G. D., & Critical Care Management Group. (2007). An 18-yr prospective study of pediatric diabetic ketoacidosis: an approach to minimizing the risk of brain herniation during treatment. Pediatric Diabetes, 8(3), 142–149. doi:10.1111/j.1399-5448.2007.00253.x Poirier, M. P., Greer, D., & Satin-Smith, M. (2004). A prospective study of the "two-bag system’’ in diabetic ketoacidosis management. Clinical Pediatrics, 43(9), 809–813. Rosenbloom, A. L. (2010). The management of diabetic ketoacidosis in children. Diabetes Therapy, 1(2), 103–120. doi:10.1007/s13300-010-0008-2 Savage, M. W., Dhatariya, K. K., Kilvert, A., Rayman, G., Rees, J. A. E., Courtney, C. H., … Joint British Diabetes Societies. (2011). Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Medicine: A Journal of the British Diabetic Association, 28(5), 508–515. doi:10.1111/j.1464-5491.2011.03246.x Silverstein, J., Klingensmith, G., Copeland, K., Plotnick, L., Kaufman, F., Laffel, L., … American Diabetes Association. (2005). Care of children and adolescents with type 1 diabetes: a statement of the American Diabetes Association. Diabetes Care, 28(1), 186–212. So, T.-Y., & Grunewalder, E. (2009). Evaluation of the Two-Bag System for Fluid Management in Pediatric Patients with Diabetic Ketoacidosis. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 14(2), 100–105. doi:10.5863/15516776-14.2.100 Wolfsdorf, J., Glaser, N., Sperling, M. A., & American Diabetes Association. (2006). Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care, 29(5), 1150–1159. doi:10.2337/diacare.2951150 This guideline does not take into account individual patient situations, and does not substitute for clinical judgment
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