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Premium member Presentation Transcript Diabetic Ketoacidosis Management : Diabetic Ketoacidosis Management Heidi Chamberlain Shea, MD Endocrine Associates of Dallas Goals of Discussion : Goals of Discussion Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome Epidemiology : Epidemiology Annual incidence in U.S. 5-8 per 1000 diabetic subjects 2.8% of all diabetic admissions are due to DKA Overall mortality rate ranges from 2-10% Higher is older patients DKAPrecipitating Factors : DKAPrecipitating Factors Failure to take insulin Failure to increase insulin Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional Medical Stress Counterregulatory hormones Oppose insulin Stimulate glucagon release Hypovolmemia Increases glucagon and catecholamines Decreased renal blood flow Decreases glucagon degradation by the kidney Diabetic Ketoacidosis : Diabetic Ketoacidosis Due to: Severe insulin deficiency Excess counterregulatory hormones Glucagon Epinephrine Cortisol Growth hormone Role of Insulin : Role of Insulin Required for transport of glucose into Muscle Adipose Liver Inhibits lipolysis Absence of insulin Glucose accumulates in the blood Liver Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies Acetone, Acetoacetate, β-hydroxybutyrate Increased counterregulatory hormones Counterregulatory Hormones - DKA : Counterregulatory Hormones - DKA Slide 8: Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Dehydration Signs and Symptoms of DKA : Signs and Symptoms of DKA Polyuria, polydipsia Enuresis Dehydration Tachycardia Orthostasis Abdominal pain Nausea Vomiting Fruity breath Acetone Kussmaul breathing Mental status changes Combative Drunk Coma Lab Findings : Lab Findings Hyperglycemia Anion gap acidosis (Na + K) – (Cl + Bicarb) >12 Bicarbonate <15 mEq/L pH <7.3 Urine ketones and serum ketones Hyperosmolarity Differential Diagnosis Anion Gap Acidosis : Differential Diagnosis Anion Gap Acidosis Alcoholic ketoacidosis Lactic acidosis Renal failure Ethylene glycol or methyl alcohol poisoning Starvation in late pregnancy or lactation (rare) Atypical Presentations : Atypical Presentations DKA can be present with BS <300 Impaired gluconeogenesis Liver disease Acute alcohol ingestion Prolonged fasting Insulin-independent glucose is high (pregnancy) Chronic poor control but taking insulin Bedside urine ketones false negatives Measure acetoacetate not β-hydroxybutyrate Send blood to lab Treatment of DKA : Treatment of DKA Initial hospital management Replace fluid and electrolytes IV Insulin therapy Glucose administration Watch for complications Disconnect insulin pump Once resolved Convert to home insulin regimen Prevent recurrence Treatment of DKAFluids and Electrolytes : Treatment of DKAFluids and Electrolytes Fluid replacement Restores perfusion of the tissues Lowers counterregulatory hormones Average fluid deficit 3-5 liters Initial resuscitation 1-2 liters of normal saline over the first 2 hours Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours When fluid overload is a concern If hypernatremia develops ½ NS can be used Treatment of DKAFluids and Electrolytes : Treatment of DKAFluids and Electrolytes Hyperkalemia initially present Resolves quickly with insulin drip Once urine output is present and K<5.0, add 20-40 meq KCL per liter. Phosphate deficit May want to use Kphos Bicarbonate not given unless pH <7 or bicarbonate <5 mmol/L Treatment of DKAInsulin Therapy : Treatment of DKAInsulin Therapy IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin Follow with hourly regular insulin infusion Glucose levels Decrease 75-100 mg/dl hour Minimize rapid fluid shifts Continue IV insulin until urine is free of ketones Treatment of DKAGlucose Administration : Treatment of DKAGlucose Administration Supplemental glucose Hypoglycemia occurs Insulin has restored glucose uptake Suppressed glucagon Prevents rapid decline in plasma osmolality Rapid decrease in insulin could lead to cerebral edema Glucose decreases before ketone levels decrease Start glucose when plasma glucose <300 mg/dl Insulin-Glucose Infusion for DKA : Insulin-Glucose Infusion for DKA Complications of DKA : Complications of DKA Infection Precipitates DKA Fever Leukocytosis can be secondary to acidosis Shock If not improving with fluids r/o MI Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days after DKA Pulmonary Edema Result of aggressive fluid resuscitation Cerebral Edema First 24 hours Mental status changes Tx: Mannitol May require intubation with hyperventilation Once DKA ResolvedTreatment : Once DKA ResolvedTreatment Most patients require 0.5-0.6 units/kg/day Pubertal or highly insulin resistant patients 0.8-1.0 units/kg/day Long acting insulin 1/2-2/3 daily requirement NPH, Lente, Ultralente or Lantus Short acting insulin 1/3-1/2 given at meals Regular, Humalog, Novolog Give insulin at least 2 hours prior to weaning insulin infusion. Prevention of DKASick Day Rules : Prevention of DKASick Day Rules Never omit insulin Cut long acting in half Prevent dehydration and hypoglycemia Monitor blood sugars frequently Monitor for ketosis Provide supplemental fast acting insulin Treat underlying triggers Maintain contact with medical team Goals of Discussion : Goals of Discussion Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome Hyperosmolar Nonketotic Syndrome : Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and dehydration Unable to excrete glucose as quickly as it enters the extracellular space Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space. Hyperosmolar Nonketotic Syndrome : Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and hyperosmolarity High mortality (12-46%) At risk Older patients with intercurrent illness Impaired ability to ingest fluids Urine volume falls Decreased glucose excretion Elevated glucose causes CNS dysfunction and fluid intake impaired No ketones Some insulin may be present Extreme hyperglycemia inhibits lipolysis Hyperosmolar Nonketotic Syndrome Presentation : Hyperosmolar Nonketotic Syndrome Presentation Extreme dehydration Supine or orthostatic hypotension Confusion coma Neurological findings Seizures Transient hemiparesis Hyperreflexia Generalized areflexia Hyperosmolar Nonketotic Syndrome Presentation : Hyperosmolar Nonketotic Syndrome Presentation Glucose >600 mg/dl Sodium Normal, elevated or low Potassium Normal or elevated Bicarbonate >15 mEq/L Osmolality >320 mOsm/L Hyperosmolar Nonketotic Syndrome Treatment : Hyperosmolar Nonketotic Syndrome Treatment Fluid repletion NS 2-3 liters rapidly Total deficit = 10 liters Replete ½ in first 6 hours Insulin Make sure perfusion is adequate Insulin drip 0.1U/kg/hr Treat underlying precipitating illness Clinical Errors : Clinical Errors Fluid shift and shock Giving insulin without sufficient fluids Using hypertonic glucose solutions Hyperkalemia Premature potassium administration before insulin has begun to act Hypokalemia Failure to administer potassium once levels falling Recurrent ketoacidosis Premature discontinuation of insulin and fluids when ketones still present Hypoglycemia Insufficient glucose administration Conclusion : Conclusion Successful management requires Judicious use of fluids Establish good perfusion Insulin drip Steady decline Complete resolution of ketosis Electrolyte replacement Frequent neurological evaluations High suspicion for complications Determine etiology to avoid recurrent episodes You do not have the permission to view this presentation. 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Diabetic Ketoacidosis Management audam Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 1661 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: December 02, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Diabetic Ketoacidosis Management : Diabetic Ketoacidosis Management Heidi Chamberlain Shea, MD Endocrine Associates of Dallas Goals of Discussion : Goals of Discussion Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome Epidemiology : Epidemiology Annual incidence in U.S. 5-8 per 1000 diabetic subjects 2.8% of all diabetic admissions are due to DKA Overall mortality rate ranges from 2-10% Higher is older patients DKAPrecipitating Factors : DKAPrecipitating Factors Failure to take insulin Failure to increase insulin Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional Medical Stress Counterregulatory hormones Oppose insulin Stimulate glucagon release Hypovolmemia Increases glucagon and catecholamines Decreased renal blood flow Decreases glucagon degradation by the kidney Diabetic Ketoacidosis : Diabetic Ketoacidosis Due to: Severe insulin deficiency Excess counterregulatory hormones Glucagon Epinephrine Cortisol Growth hormone Role of Insulin : Role of Insulin Required for transport of glucose into Muscle Adipose Liver Inhibits lipolysis Absence of insulin Glucose accumulates in the blood Liver Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies Acetone, Acetoacetate, β-hydroxybutyrate Increased counterregulatory hormones Counterregulatory Hormones - DKA : Counterregulatory Hormones - DKA Slide 8: Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Dehydration Signs and Symptoms of DKA : Signs and Symptoms of DKA Polyuria, polydipsia Enuresis Dehydration Tachycardia Orthostasis Abdominal pain Nausea Vomiting Fruity breath Acetone Kussmaul breathing Mental status changes Combative Drunk Coma Lab Findings : Lab Findings Hyperglycemia Anion gap acidosis (Na + K) – (Cl + Bicarb) >12 Bicarbonate <15 mEq/L pH <7.3 Urine ketones and serum ketones Hyperosmolarity Differential Diagnosis Anion Gap Acidosis : Differential Diagnosis Anion Gap Acidosis Alcoholic ketoacidosis Lactic acidosis Renal failure Ethylene glycol or methyl alcohol poisoning Starvation in late pregnancy or lactation (rare) Atypical Presentations : Atypical Presentations DKA can be present with BS <300 Impaired gluconeogenesis Liver disease Acute alcohol ingestion Prolonged fasting Insulin-independent glucose is high (pregnancy) Chronic poor control but taking insulin Bedside urine ketones false negatives Measure acetoacetate not β-hydroxybutyrate Send blood to lab Treatment of DKA : Treatment of DKA Initial hospital management Replace fluid and electrolytes IV Insulin therapy Glucose administration Watch for complications Disconnect insulin pump Once resolved Convert to home insulin regimen Prevent recurrence Treatment of DKAFluids and Electrolytes : Treatment of DKAFluids and Electrolytes Fluid replacement Restores perfusion of the tissues Lowers counterregulatory hormones Average fluid deficit 3-5 liters Initial resuscitation 1-2 liters of normal saline over the first 2 hours Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours When fluid overload is a concern If hypernatremia develops ½ NS can be used Treatment of DKAFluids and Electrolytes : Treatment of DKAFluids and Electrolytes Hyperkalemia initially present Resolves quickly with insulin drip Once urine output is present and K<5.0, add 20-40 meq KCL per liter. Phosphate deficit May want to use Kphos Bicarbonate not given unless pH <7 or bicarbonate <5 mmol/L Treatment of DKAInsulin Therapy : Treatment of DKAInsulin Therapy IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin Follow with hourly regular insulin infusion Glucose levels Decrease 75-100 mg/dl hour Minimize rapid fluid shifts Continue IV insulin until urine is free of ketones Treatment of DKAGlucose Administration : Treatment of DKAGlucose Administration Supplemental glucose Hypoglycemia occurs Insulin has restored glucose uptake Suppressed glucagon Prevents rapid decline in plasma osmolality Rapid decrease in insulin could lead to cerebral edema Glucose decreases before ketone levels decrease Start glucose when plasma glucose <300 mg/dl Insulin-Glucose Infusion for DKA : Insulin-Glucose Infusion for DKA Complications of DKA : Complications of DKA Infection Precipitates DKA Fever Leukocytosis can be secondary to acidosis Shock If not improving with fluids r/o MI Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days after DKA Pulmonary Edema Result of aggressive fluid resuscitation Cerebral Edema First 24 hours Mental status changes Tx: Mannitol May require intubation with hyperventilation Once DKA ResolvedTreatment : Once DKA ResolvedTreatment Most patients require 0.5-0.6 units/kg/day Pubertal or highly insulin resistant patients 0.8-1.0 units/kg/day Long acting insulin 1/2-2/3 daily requirement NPH, Lente, Ultralente or Lantus Short acting insulin 1/3-1/2 given at meals Regular, Humalog, Novolog Give insulin at least 2 hours prior to weaning insulin infusion. Prevention of DKASick Day Rules : Prevention of DKASick Day Rules Never omit insulin Cut long acting in half Prevent dehydration and hypoglycemia Monitor blood sugars frequently Monitor for ketosis Provide supplemental fast acting insulin Treat underlying triggers Maintain contact with medical team Goals of Discussion : Goals of Discussion Pathophysiology of DKA Biochemical criteria for DKA Treatment of DKA Prevention of DKA Hyperosmolar Nonketoic Syndrome Hyperosmolar Nonketotic Syndrome : Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and dehydration Unable to excrete glucose as quickly as it enters the extracellular space Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space. Hyperosmolar Nonketotic Syndrome : Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and hyperosmolarity High mortality (12-46%) At risk Older patients with intercurrent illness Impaired ability to ingest fluids Urine volume falls Decreased glucose excretion Elevated glucose causes CNS dysfunction and fluid intake impaired No ketones Some insulin may be present Extreme hyperglycemia inhibits lipolysis Hyperosmolar Nonketotic Syndrome Presentation : Hyperosmolar Nonketotic Syndrome Presentation Extreme dehydration Supine or orthostatic hypotension Confusion coma Neurological findings Seizures Transient hemiparesis Hyperreflexia Generalized areflexia Hyperosmolar Nonketotic Syndrome Presentation : Hyperosmolar Nonketotic Syndrome Presentation Glucose >600 mg/dl Sodium Normal, elevated or low Potassium Normal or elevated Bicarbonate >15 mEq/L Osmolality >320 mOsm/L Hyperosmolar Nonketotic Syndrome Treatment : Hyperosmolar Nonketotic Syndrome Treatment Fluid repletion NS 2-3 liters rapidly Total deficit = 10 liters Replete ½ in first 6 hours Insulin Make sure perfusion is adequate Insulin drip 0.1U/kg/hr Treat underlying precipitating illness Clinical Errors : Clinical Errors Fluid shift and shock Giving insulin without sufficient fluids Using hypertonic glucose solutions Hyperkalemia Premature potassium administration before insulin has begun to act Hypokalemia Failure to administer potassium once levels falling Recurrent ketoacidosis Premature discontinuation of insulin and fluids when ketones still present Hypoglycemia Insufficient glucose administration Conclusion : Conclusion Successful management requires Judicious use of fluids Establish good perfusion Insulin drip Steady decline Complete resolution of ketosis Electrolyte replacement Frequent neurological evaluations High suspicion for complications Determine etiology to avoid recurrent episodes