Presentation on theme: "Diabetic Ketoacidosis and Hyperglycemia"— Presentation transcript:
1Diabetic Ketoacidosis and Hyperglycemia Valerie Robinson, D.O.
2Hyperglycemia Type 1 DM, Type 2 DM, Gestational Diabetes May present with polyuria, polydipsia, weight lossMay present with DKAType 1: usually in children with rapid onset. Caused by autoimmune pancreatic ß-cell destruction, or idiopathicType 2: usually in adults with insidious onset. Caused by insulin resistance, insulin secretory defectGenetic and environmental factors influence development of hyperglycemia.The main goals of treatment are to alleviate symptoms, minimize the development of long-term complications, enhance the patient's quality of life, and reduce the risk of death.
3Complications of Hyperglycemia May lead to DKA, and Hyperosmolar Hyperglycemic State.Macrovascular disease CAD, MI, CVA, PADDiabetic foot ulcersMicrovascular disease nephropathy, retinopathy, neuropathy, Charcot’s foot, EDIncreased risk of infxns and decreased healingGestational preeclampsia, SAB, premature labor, polyhydramnios, macrosomia, RDS
4What is DKA? Severe electrolyte imbalance with dehydration Severe insulin shortageUsually occurs in type 1 but may also occur in type 2May be the initial presentation of diabetes mellitusMay be brought on by an infection or another precipitating factortrauma, CVD, pancreatitis, drugs, ETOH, poor diet
5Signs and Symptoms Fruity odor to breath (exhaled acetone) Shock Abdominal pain (ileus or delayed emptying)Altered consciousnessNausea/VomitingDehydrationPolyuriaPolydipsiaKussmaul breathing (compensatory hyperventilation)
6PathogenesisPancreatic islet cells are destroyed, resulting in a lack of insulin and hyperglycemia.Hyperglycemia induces profound osmotic diuresis, causing water and electrolyte loss, especially potassium.The body cannot properly use extracellular glucose, so starts producing ketones as an alternate energy source.Ketosis causes metabolic acidosis.Metabolic acidosis forces hydrogen ions into cells, displacing potassium ions that are lost through urine and vomiting. Increased anion gap: Usu. >20meq/L
7Pathogenesis cont.Total-body potassium depletion is present, but serum potassium levels may be normal or high because of electrolyte shiftExtreme fluid loss results in clinical shockIn some cases, hyperglycemia and dehydration predominate, and acidosis is minimal
8Tests Results When you suspect DKA, order the following: FSBS/serum glucose- Used serially to follow tx progressUrine or serum ketonesABGBMPK+ must be monitored closelyBUN/Cr used to follow tx progressCBCBlood cultures>250 mg/dL rarely >800 mg/dLHigh levels confirm dxpH < pCO2 <40 mmHg- confirms dx, reveals severityK+ may be high or normal- K+ may fall rapidly in tx- BUN/Cr reveal dehydrationLeukocytosisPossible sepsis
9Tests cont. Results cont. Serum Phosphate, Ca, Mg Amylase/lipase LFTs You may choose to order the followingSerum Phosphate, Ca, MgAmylase/lipaseLFTsDo if c/o abdominal painEKGCXRLipidsMay be decreased.- May decrease during txMay be elevated in DKA- May indicate pancreatitisNot usually elevated in DKALook for peaked T or U waves- Look for evidence of precipitating eventLook for precipitating eventLikely elevated – aid in ketogenesis
10Diagnosis pH <7.3 Hyperglycemia Ketonuria Dehydration Patient may be asymptomatic, but should still be treated before symptoms occur.
11Treatment #1: HYDRATION Hydration with NS. Calculate fluid deficit. Assume 5-10% dehydration if patient is acidotic.Correct over hours.Usually mL bolus in first hourChildren 10-20mL/kg bolus. May use NS, crystalloid, or LR
12Treatment #2: Insulin Bolus of 0.1 Units/kg IV Then 0.1 Units/kg/hour IVChildren: no insulin bolus Units/kg/hour IVOR (in mild DKA or long transport)Short-acting insulinInitial dose 0.3 Units/kg SQThen 0.1 Units/kg/hour SQ until glucose <250 mg/dLThen 0.05 Units/kg/hour SQ until DKA is resolvedChildren: no insulin bolus Units/kg/2hours SQ or IMCaution: Do not reduce serum glucose by more than80 mg/dL/hour in children, mg/dL/hour in adults
13Treatment #3: Potassium 20-40 meq/L added to the IV NSTitrated to serum K+ concentrationsUsually added after assured of urine output
14Other TreatmentBicarbonate may worsen hypokalemia and intracellular acidosis and cause cerebral edema.Used in ICU when pH <6.9Sodium phosphate is not used routinely.Tx if: <1 mg/dL OR significant cardiac or respiratory compromise.Dextrose 5% if glucose falls too rapidly and when it falls <250mg/dL. Don’t stop insulin until acidosis is corrected.Caution: If you fail to monitor and replace electrolytes, rehydrate too fast, or reduce glucose too fast, you may cause cerebral edema.If + cerebral edema, do not replace more than 75% of fluid deficitMay use mannitol g/kg over 20 minutes
15Follow-up Look for a cause of the DKA Make sure glucose is well-controlled at home and patient is educated regarding DKA.
16Non-Ketotic Hyperosmolar Coma Hyperosmolar Hyperglycemic StateLevel of consciousness is depressed when plasma osmolality is highMay be precipitated by concomitant use of certain quinolone antibiotics in patients with diabetes taking certain oral hypoglycemic agentsMarkedly elevated plasma osmolalitySevere hyperglycemia >600 mg/dL, may exceed 1000 mg/dLNo significant ketonuria/ketonemiaNo significant acidosis, pH >7.3 and bicarbonate >15meq/LUsually occurs in elderly patients who often have undiagnosed DM2Thromboembolic complications are commonInsulin requirement is less than that for DKARequires ICU monitoring
17ReferencesDavid Toth MD et al. Gestational Diabetes. First Consult . 29 January 2010Dennis Saver MD et al. Diabetic Ketoacidosis. First Consult. 27 April 2010.Abbas E. Kitabchi MD, PhD et al. Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. UpToDate. 25 June 2012.