Presentation is loading. Please wait.

Presentation is loading. Please wait.

Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State (2012) Author(s): Jennifer N.

Similar presentations


Presentation on theme: "Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State (2012) Author(s): Jennifer N."— Presentation transcript:

1 Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State (2012) Author(s): Jennifer N. Thompson, M.D., Project Hope License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1

2 Attribution Key for more information see: Use + Share + Adapt Make Your Own Assessment Creative Commons – Attribution License Creative Commons – Attribution Share Alike License Creative Commons – Attribution Noncommercial License Creative Commons – Attribution Noncommercial Share Alike License GNU – Free Documentation License Creative Commons – Zero Waiver Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (17 USC § 102(b)) *laws in your jurisdiction may differ Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Government: Works that are produced by the U.S. Government. (17 USC § 105) Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (17 USC § 107) *laws in your jurisdiction may differ Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that your use of the content is Fair. To use this content you should do your own independent analysis to determine whether or not your use will be Fair. { Content the copyright holder, author, or law permits you to use, share and adapt. } { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } { Content Open.Michigan has used under a Fair Use determination. } 2

3 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State Jennifer N. Thompson, MD Project Hope Pathophysiology of diabetic ketoacidosis 3

4 Objectives DKA: Diabetic Ketoacidosis HHS: Hyperosmolar Hyperglycemic State (HONKC – hyperosmolar nonketotic coma) (HONKC – hyperosmolar nonketotic coma) What is the difference between DKA and HHS? What is the difference between DKA and HHS? How do I manage DKA and HHS? How do I manage DKA and HHS? What complications should I look out for? What complications should I look out for? What does the data say about cerebral edema? What does the data say about cerebral edema? 4

5 Definitions Diabetic Ketoacidosis HHS - Hyperosmolar hyperglycemic state Blood glucoseGlucose >250 (13.9)Glucose >600 (33.3) Arterial pHpH <7.3pH >7.3 Serum Bicarbonate<15>15 Serum osmolalityvaries>320 mOsm Urine ketones+++Small or none Anion gap>12 DemographicsMostly type I DM Children, young people Mostly type II DM Elderly, mentally or physically impaired Insulin activityAbsolute functional insulin deficiency Relative insulin deficiency Mortality in admitted patients 1-4%10% or more 5

6 Classic presentation of DKA Age Young people, Type I DM Young people, Type I DMHistory Polydipsia, Polyuria, Fatigue Polydipsia, Polyuria, Fatigue Nausea/vomiting, diffuse abdominal pain. Nausea/vomiting, diffuse abdominal pain. In severe cases – lethargy, confusion In severe cases – lethargy, confusionPhysical Ill appearance Ill appearance Signs of dehydration: Dry skin, dry mucous membranes, decreased skin turgor (skin tenting) Signs of dehydration: Dry skin, dry mucous membranes, decreased skin turgor (skin tenting) Signs of acidosis: Signs of acidosis: Tachypnea  Kussmaul respirations Tachypnea  Kussmaul respirations Characteristic acetone (ketotic) breath odor Characteristic acetone (ketotic) breath odor 6

7 Role of Insulin Required for transport of glucose into cells for use in making ATP Required for transport of glucose into cells for use in making ATP Muscle Muscle Adipose Adipose Liver Liver Inhibits lipolysis Inhibits lipolysis Type I DM = inadequate insulin Type I DM = inadequate insulin 7 Source Undetermined

8 Pathophysiology in DKA Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Insulin Counterregulatory hormones Glucagon Epinephrine Cortisol Growth Hormone 8

9 Counterregulatory Hormones - DKA Increases insulin resistance Activates glycogenolysis and gluconeogenesis Activates lipolysis Inhibits insulin secretion Epinephrine XXXX Glucagon X Cortisol XX Growth Hormone XXX 9

10 Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Dehydration  No Liploysis = No Ketoacidosis  Only a small amount of functional insulin required to suppress lipolysis 10

11 Underling stressors that tip the balance Newly diagnosed diabetics Newly diagnosed diabetics Missed insulin treatments Missed insulin treatments Dehydration Dehydration Underlying infection Underlying infection Other physiologic stressors: Other physiologic stressors: Ex) Pulmonary embolism, Illicit drug use (sympathomimetics), Stroke, Acute Myocardial Infarction, Ex) Pulmonary embolism, Illicit drug use (sympathomimetics), Stroke, Acute Myocardial Infarction, Young type II diabetics with stressors Young type II diabetics with stressors 11 Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Insulin Glucagon Epinephrine Cortisol Growth Hormone Pathophysiology

12 Workup Most important labs to diagnose DKA: Basic metabolic panel (glucose, anion gap, potassium) Basic metabolic panel (glucose, anion gap, potassium) Arterial or venous blood gas to follow pH Arterial or venous blood gas to follow pH Urine dipstick for glucose and ketones (high sensitivity, high negative predictive value) Urine dipstick for glucose and ketones (high sensitivity, high negative predictive value) Additional tests: Additional tests: Serum ketones Serum ketones Magnesium, phosphorus Magnesium, phosphorus EKG – if you suspect hyperkalemia, hypokalemia, arrhythmias EKG – if you suspect hyperkalemia, hypokalemia, arrhythmias **Determine the underlying cause! 12

13 Management Fluids Fluids Insulin Insulin Electrolyte repletion Electrolyte repletion Find and treat any underlying cause! Find and treat any underlying cause! 13

14 Fluids Increases intravascular volume Increases intravascular volume Reverses dehydration Reverses dehydration Restores perfusion to kidneys   GFR  urinate out excess glucose Restores perfusion to kidneys   GFR  urinate out excess glucose Restores perfusion to periphery   uptake and use of glucose (when insulin present) Restores perfusion to periphery   uptake and use of glucose (when insulin present) Take home message: Fluids hydrate patient AND reverse hyperglycemia 14

15 Fluids Pediatrics Hypotension: treat with 20cc/kg NS boluses Hypotension: treat with 20cc/kg NS boluses If no hypotension: If no hypotension: 10-20cc/kg NS bolus then 1.5 – 2x maintenance 10-20cc/kg NS bolus then 1.5 – 2x maintenanceOR Assume 10% dehydration and calculate fluid deficit plus maintenance Assume 10% dehydration and calculate fluid deficit plus maintenance Replete deficit (plus maintenance) over 48-72hrs. Replete deficit (plus maintenance) over 48-72hrs. 15

16 Insulin Allows glucose to enter and be used by cells Allows glucose to enter and be used by cells Stops proteolysis and lipolysis Stops proteolysis and lipolysis  Stops Ketogenesis  Stops Acidosis Allows potassium to enter cells Allows potassium to enter cells Insulin goal: Treat the anion gap acidosis (not the hyperglycemia) (not the hyperglycemia) Never stop the insulin before the anion gap is closed. Never stop the insulin before the anion gap is closed. 16

17 Insulin Dosing: 0.05 units/kg bolus then.05 units/kg/hr insulin drip. (Previously 0.1 units/kg/hr) Dosing: 0.05 units/kg bolus then.05 units/kg/hr insulin drip. (Previously 0.1 units/kg/hr) Goal: Decrease glucose by <100 (5.5) per hour Goal: Decrease glucose by <100 (5.5) per hour Avoids sudden fluid shifts that may lead to cerebral edema Avoids sudden fluid shifts that may lead to cerebral edema Reason for IV insulin Reason for IV insulin Not affected by decreased peripheral circulation as with subcutaneous insulin Not affected by decreased peripheral circulation as with subcutaneous insulin Smooth decline of glucose Smooth decline of glucose Short half-life allows for more precise control of serum insulin concentration Short half-life allows for more precise control of serum insulin concentration 17

18 Insulin If pt has an anion gap and your glucose is <250 (14), do you stop the insulin drip? If pt has an anion gap and your glucose is <250 (14), do you stop the insulin drip? NO! NO! Add D5 when glucose <250 (14). Add D5 when glucose <250 (14). If glucose <150 (8.3), consider D10. If glucose <150 (8.3), consider D10. TAKE HOME POINT: Do not stop insulin until anion gap is closed. Do not stop insulin until anion gap is closed. Main goal of insulin therapy is to fix the acidosis. Main goal of insulin therapy is to fix the acidosis. 18

19 Transitioning to Subcutaneous Insulin ONLY after the Anion Gap is closed! ONLY after the Anion Gap is closed! OVERLAP IV and subcutaneous insulin administration OVERLAP IV and subcutaneous insulin administration Give long-acting insulin dose (ex. lantus) at least 30 to 60 minutes prior to stopping insulin drip. Give long-acting insulin dose (ex. lantus) at least 30 to 60 minutes prior to stopping insulin drip. Feed patient Feed patient 19

20 Managing electrolytes Potassium Potassium Sodium Sodium Phosphorus Phosphorus Glucose Glucose 20

21 Electrolyte management Potassium Total Body Potassium depletion Acidosis  K + exits cells as H + enters to buffer Acidosis  K + exits cells as H + enters to buffer Dehydration and volume depletion Dehydration and volume depletion Osmotic diuresis +  aldosterone  loss of K+ Osmotic diuresis +  aldosterone  loss of K+ è Although serum K + is usually normal or high, total body K + is low. 21

22 Electrolyte Management Potassium With insulin therapy With insulin therapy K + moves into cells K + moves into cells To avoid hypokalemia To avoid hypokalemia Give oral and/or IV potassium to avoid hypokalemia when K < 4.5 Give oral and/or IV potassium to avoid hypokalemia when K < 4.5 Monitor K + levels and EKG Monitor K + levels and EKG Low K – Biphasic T, U-wave Low K – Biphasic T, U-wave High K - tall peaked T, flat P waves, wide QRS High K - tall peaked T, flat P waves, wide QRS Cardiac dysrhythmia Cardiac dysrhythmia 22

23 Electrolyte Management Sodium Pseudohyponatremia: For each 100mg/dl increase of glucose above 100, For each 100mg/dl increase of glucose above 100, Na + decreases by 1.6 mEq/L Na + decreases by 1.6 mEq/L Corrected Na + = measured Na + Corrected Na + = measured Na meq/L x (glucose-100)/100)) 1.6 meq/L x (glucose-100)/100)) Example: Example: Na + = 125 meq/L and Glucose = 500 mg/dl 500 – 100 = /100 = 4 4 x 1.6 = 6.4 meq/L Corrected Na + = = meq/L 23

24 **Electrolyte Management Phosphorus Hypophosphatemia Occurs after aggressive hydration/treatment Occurs after aggressive hydration/treatment Monitor phosphorus and replete as needed to keep > 1 Monitor phosphorus and replete as needed to keep > 1 Total body phosphorus depleted Total body phosphorus depleted Mostly a theoretical problem Mostly a theoretical problem Potential complications: muscle weakness, myocardial dysfunction, CNS depression Potential complications: muscle weakness, myocardial dysfunction, CNS depression 24

25 Management review Rehydrate patient with IV fluids Rehydrate patient with IV fluids Continue insulin drip until anion gap is closed Continue insulin drip until anion gap is closed Until insulin drip is off: Until insulin drip is off: Check glucose every hour. Avoid hypoglycemia. Check glucose every hour. Avoid hypoglycemia. Check electrolytes every 1-2hrs. Avoid hypokalemia. Check electrolytes every 1-2hrs. Avoid hypokalemia. Replete potassium when K < 4.5 and patient making urine Replete potassium when K < 4.5 and patient making urine 25

26 ICU Monitoring Careful nursing monitoring of the following: I/Os (input and urine output.) I/Os (input and urine output.) Urine dipstick with every void Urine dipstick with every void resolution of ketonuria may lag behind clinical improvement resolution of ketonuria may lag behind clinical improvement Monitor for any signs of cerebral edema: Monitor for any signs of cerebral edema: Change in mental status, severe headache Change in mental status, severe headache Sudden drop in heart rate Sudden drop in heart rate Neurologic deficits Neurologic deficits 26

27 DKA Complications Dehydration, shock, hypotension Dehydration, shock, hypotension Hypokalemia/ hyperkalemia Hypokalemia/ hyperkalemia Hypoglycemia Hypoglycemia Aspiration pneumonia Aspiration pneumonia Sepsis Sepsis Acute tubular necrosis Acute tubular necrosis Myocardial infarction Myocardial infarction Stroke Stroke Cerebral edema Cerebral edema * Death rate in U.S when managed in hospital setting = 1-4% = 1-4% 27

28 DKA Complications Cerebral edema Clinical manifestations: Clinical manifestations: Altered mental status Altered mental status Headache Headache Persistent vomiting Persistent vomiting Sudden and persistent drop in heart rate Sudden and persistent drop in heart rate Seizure Seizure Unequal or fixed, dilated pupils Unequal or fixed, dilated pupils Mostly children Mostly children High mortality rate High mortality rate 1% of DKA pts, > 25% mortality rate 1% of DKA pts, > 25% mortality rate High morbidity rate High morbidity rate High rate of neurologic complications High rate of neurologic complications 28

29 DKA Complications Cerebral edema Risk Factors Risk Factors Age < 5 years Age < 5 years More often seen in your sickest patients More often seen in your sickest patients (high BUN, low bicarb <15) (high BUN, low bicarb <15) Fall in serum Na or lack of increase during treatment Fall in serum Na or lack of increase during treatment Rapid correction of hyperglycemia Rapid correction of hyperglycemia Goal: decrease glucose <100 mg/dl (5.5) per hour Goal: decrease glucose <100 mg/dl (5.5) per hour Sodium bicarbonate administration Sodium bicarbonate administration Excessive fluids Excessive fluids 29

30 DKA Complications Cerebral Edema - treatment Mannitol 1mg/kg IV Mannitol 1mg/kg IV Reduce IV fluid rate (ex. 70% maintenance) Reduce IV fluid rate (ex. 70% maintenance) Consider intubation Consider intubation set the ventilator close to rate that patient was breathing beforehand set the ventilator close to rate that patient was breathing beforehand be cautious of over hyperventilation be cautious of over hyperventilation Temporary measure Temporary measure Keep pCO2 > 22mmHg Keep pCO2 > 22mmHg May consider 3% hypertonic saline May consider 3% hypertonic saline but not enough data to truly recommend but not enough data to truly recommend 30

31 Definitions Diabetic Ketoacidosis HHS - Hyperosmolar hyperglycemic state) (AKA HONKC = hyperosmolar nonketotic coma) Blood glucoseGlucose >250 (13.9)Glucose >600 (33.3) Arterial pHpH <7.3pH >7.3 Serum Bicarbonate<15>15 Serum osmolalityvaries>320 mOsm Urine ketones+++small Anion gap>12 DemographicsMostly type I DM Children, young people Mostly type II DM Elderly Insulin activityAbsolute functional insulin deficiency Relative insulin deficiency Mortality in admitted patients 1-4%10% or more 31

32 HHS (Hyperosmolar Hyperglycemic State) Elderly and mentally or physically impaired patients Elderly and mentally or physically impaired patients Usually associated with underlying physiologic stressors Usually associated with underlying physiologic stressors Ex. Infection, myocardial infarction, stroke. Ex. Infection, myocardial infarction, stroke. Slower onset (ex. 1 week vs. 1-2 days in DKA) Slower onset (ex. 1 week vs. 1-2 days in DKA) Higher Mortality rate than DKA (>10%) Higher Mortality rate than DKA (>10%) Older patients, more comorbidities Older patients, more comorbidities Presentation: Altered mental status (confusion, neurologic deficits) Altered mental status (confusion, neurologic deficits) Signs of severe dehydration (tachycardia, hypotension, dry mucous membranes, skin tenting) Signs of severe dehydration (tachycardia, hypotension, dry mucous membranes, skin tenting) 32

33 Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Dehydration  No Liploysis = No Ketoacidosis  Only a small amount of functional insulin required to suppress lipolysis  Low catecholamine levels in elderly patients  less insulin resistance 33

34 HHS - State of severe dehydration Therapy: Fluid repletion Fluid repletion Total fluid deficit ≈ 10 liters in adults Total fluid deficit ≈ 10 liters in adults Normal saline 2-3 liters rapidly Normal saline 2-3 liters rapidly Replete ½ in first 6 hours Replete ½ in first 6 hours Insulin drip 0.05 units/kg/hr Insulin drip 0.05 units/kg/hr Decrease glucose by approximately 50 mEQ/hr Decrease glucose by approximately 50 mEQ/hr Check electrolytes q1-2hrs. Check glucose q1hr Check electrolytes q1-2hrs. Check glucose q1hr Monitor potassium for hypokalemia/hyperkalemia Monitor potassium for hypokalemia/hyperkalemia Treat underlying precipitating illness Treat underlying precipitating illness Potential complications are the same as DKA Potential complications are the same as DKA 34

35 Summary Pathophysiologic difference between DKA and HHS Pathophysiologic difference between DKA and HHS DKA is a state of absolute functional insulin deficiency DKA is a state of absolute functional insulin deficiency Only in DKA : Lipolysis  ketogenesis  acidosis Only in DKA : Lipolysis  ketogenesis  acidosis You are never specifically treating the glucose You are never specifically treating the glucose In DKA – you are treating the underlying acidosis/ketogenesis (reflected by the anion gap) In DKA – you are treating the underlying acidosis/ketogenesis (reflected by the anion gap) In HHS – you are treating the underlying shock caused by poor tissue perfusion/severe dehydration In HHS – you are treating the underlying shock caused by poor tissue perfusion/severe dehydration 35

36 Summary (continued) Being too aggressive in management may cause more harm than good Being too aggressive in management may cause more harm than good If you don’t pay attention to details, you will cause an iatrogenic death If you don’t pay attention to details, you will cause an iatrogenic death Monitor electrolytes (especially potassium) Monitor electrolytes (especially potassium) Beware cerebral edema. Beware cerebral edema. Therapy for DKA and HHS is similar. Therapy for DKA and HHS is similar. 36

37 Thank you diabetees.spreadshirt.com 37

38 Pathophysiology of diabetic ketoacidosis 38 Source Undetermined

39  -cell destruction Insulin Deficiency Muscle Liver Decreased Glucose Utilization & Increased Production Glucagon Increased Lipolysis Hyperglycemia Ketoacidosis HyperTG Polyuria Volume Depletion Ketonuria Amino Acids FattyAcids Stress Epi,Cortisol GH Threshold 180 mg/dl 39 Increased Ketogenesis, Gluconeogenesis, Glycogenolysis Islets of Langerhans Increased Protein Catabolism

40 40 Attributions for Slide 39: Islets of Langerhans: Afferent (WikimediaCommons)Afferent (WikimediaCommons) Adipocytes: DBCLS (WikimediaCommons)DBCLS (WikimediaCommons) Muscle: Jeremy Kemp (WikimediaCommons)Jeremy Kemp (WikimediaCommons) Liver: Mikael Haggstrom (WikimediaCommons)Mikael Haggstrom (WikimediaCommons) Kidney: Holly Fischer (WikimediaCommons)Holly Fischer (WikimediaCommons) Additional Information


Download ppt "Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State (2012) Author(s): Jennifer N."

Similar presentations


Ads by Google