GEMC: Diabetic Ketoacidosis: Resident Training

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This is a lecture by Dr. Jennifer Thompson from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.

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GEMC: Diabetic Ketoacidosis: Resident Training

  1. 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: http://creativecommons.org/licenses/by-sa/3.0/ 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 open.michigan@umich.edu with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. 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. 2. Attribution Key for more information see: http://open.umich.edu/wiki/AttributionPolicy Use + Share + Adapt { Content the copyright holder, author, or law permits you to use, share and adapt. } Public Domain – Government: Works that are produced by the U.S. Government. (17 USC § 105) Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Creative Commons – Zero Waiver 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 Make Your Own Assessment { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (17 USC § 102(b)) *laws in your jurisdiction may differ { Content Open.Michigan has used under a Fair Use determination. } 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. 2  
  3. 3. Diabetic   Ketoacidosis   and   Hyperosmolar   Hyperglycemic   State   Jennifer  N.  Thompson,  MD   Project  Hope   3  
  4. 4. Objectives   DKA:    Diabetic  Ketoacidosis   HHS:    Hyperosmolar  Hyperglycemic  State                (HONKC  –  hyperosmolar  nonketotic  coma)     l  What  is  the  difference  between  DKA  and  HHS?   l  How  do  I  manage  DKA  and  HHS?   l  What  complications  should  I  look  out  for?   l  What  does  the  data  say  about  cerebral  edema?     4  
  5. 5. Diabetic   Ketoacidosis   HHS  -­‐  Hyperosmolar   hyperglycemic  state     Blood  glucose   Glucose  >250  (13.9)   Glucose  >600  (33.3)   Arterial  pH   pH  <7.3   pH  >7.3   Serum  Bicarbonate   <15   >15   Serum  osmolality   varies   >320  mOsm   Urine  ketones   +++   Small  or  none     Anion  gap   >12   Demographics   Mostly  type  I  DM   Children,  young  people   Mostly  type  II  DM   Elderly,  mentally  or  physically   impaired   Insulin  activity   Absolute  functional   insulin  deficiency   Relative  insulin  deficiency   Mortality  in  admitted   patients   1-­‐4%   10%  or  more   Definitions     5  
  6. 6. Classic  presentation  of  DKA   l  Young  people,  Type  I  DM   Age   History   l  Polydipsia,  Polyuria,  Fatigue   l  Nausea/vomiting,  diffuse  abdominal  pain.     l  In  severe  cases  –  lethargy,  confusion     Physical   l  Ill  appearance   l  Signs  of  dehydration:  Dry  skin,  dry  mucous  membranes,   decreased  skin  turgor  (skin  tenting)   l  Signs  of  acidosis:   l  Tachypnea      Kussmaul  respirations   l  Characteristic  acetone  (ketotic)  breath  odor   6  
  7. 7. Role  of  Insulin   l  Required  for  transport  of  glucose  into  cells  for  use   in  making  ATP   l  Muscle   l  Adipose   l  Liver     l  Inhibits  lipolysis   l  Type  I  DM  =  inadequate  insulin     7   Source  Undetermined  
  8. 8. Pathophysiology  in   DKA   Counterregulatory Insulin       hormones   Glucagon   Epinephrine   Cortisol   Growth  Hormone       Gluconeogenesis   Glycogenolysis   Lipolysis   8   Ketogenesis  
  9. 9. Counterregulatory  Hormones  -­‐  DKA   Increases insulin resistance Epinephrine Activates glycogenolysis and gluconeogenesis Activates lipolysis Inhibits insulin secretion X X X X X X Glucagon X Cortisol X Growth Hormone X X 9  
  10. 10. Insulin  Deficiency   Glucose  uptake   Lipolysis   Proteolysis   Glycerol   Free  Fatty  Acids   Amino  Acids   Hyperglycemia   Gluconeogenesis   Glycogenolysis   Ketogenesis   Osmotic  diuresis   Dehydration   Acidosis   ² No  Liploysis  =  No  Ketoacidosis   ² Only a small amount of functional insulin required to suppress lipolysis   10  
  11. 11. Underling  stressors  that  tip  the  balance   Pathophysiology   l  Newly  diagnosed  diabetics   Insulin   l  Missed  insulin  treatments   Glucagon   Epinephrine   Cortisol   Growth  Hormone   l  Dehydration   l  Underlying  infection   l  Other  physiologic  stressors:   l  Ex)  Pulmonary  embolism,     Illicit  drug  use   (sympathomimetics),  Stroke,   Acute  Myocardial  Infarction,     Gluconeogenesis   Glycogenolysis   Lipolysis   Ketogenesis   l  Young  type  II  diabetics  with   stressors   11  
  12. 12. Workup   Most  important  labs  to  diagnose  DKA:   l  Basic  metabolic  panel  (glucose,  anion  gap,  potassium)   l  Arterial  or  venous  blood  gas  to  follow  pH   l  Urine  dipstick  for  glucose  and  ketones  (high  sensitivity,    high  negative   predictive  value)   l  l  l  l  Additional  tests:   Serum  ketones   Magnesium,  phosphorus   EKG  –  if  you  suspect  hyperkalemia,  hypokalemia,  arrhythmias   **Determine  the  underlying  cause!   12  
  13. 13. Management   l  Fluids   l  Insulin   l  Electrolyte  repletion   l  Find  and  treat  any  underlying  cause!   13  
  14. 14. Fluids   l  Increases  intravascular  volume   l  Reverses  dehydration   l  Restores  perfusion  to  kidneys      GFR    urinate  out  excess   glucose   l  Restores  perfusion  to  periphery      uptake  and  use  of   glucose  (when  insulin  present)     Take  home  message:    Fluids  hydrate  patient  AND  reverse  hyperglycemia   14  
  15. 15. Fluids   Pediatrics   l  Hypotension:  treat  with  20cc/kg  NS  boluses   l  If  no  hypotension:   l  10-­‐20cc/kg  NS  bolus  then  1.5  –  2x  maintenance   OR   l  Assume  10%  dehydration  and  calculate  fluid  deficit  plus   maintenance   l  Replete  deficit  (plus  maintenance)  over  48-­‐72hrs.     15  
  16. 16. Insulin   l  Allows  glucose  to  enter  and  be  used  by  cells   l  Stops  proteolysis  and  lipolysis   Ø  Stops  Ketogenesis    Stops  Acidosis   l  Allows  potassium  to  enter  cells     Insulin  goal:    Treat  the  anion  gap  acidosis                        (not  the  hyperglycemia)   l  Never  stop  the  insulin  before  the  anion  gap  is  closed.     16  
  17. 17. Insulin   l  Dosing:  0.05  units/kg  bolus  then  .05  units/kg/hr  insulin   drip.  (Previously  0.1  units/kg/hr)   l  Goal:  Decrease  glucose  by  <100  (5.5)  per  hour   l  Avoids  sudden  fluid  shifts  that  may  lead  to  cerebral  edema   l  Reason  for  IV  insulin   l  Not  affected  by  decreased  peripheral  circulation  as  with   subcutaneous  insulin   l  Smooth  decline  of  glucose   l  Short  half-­‐life  allows  for  more  precise  control  of  serum  insulin   concentration   17  
  18. 18. Insulin   l  If  pt  has  an  anion  gap  and  your  glucose  is  <250  (14),  do  you  stop   the  insulin  drip?   l  NO!     l  Add  D5  when  glucose  <250  (14).            If  glucose  <150  (8.3),  consider  D10.     TAKE  HOME  POINT:   l  Do  not  stop  insulin  until  anion  gap  is  closed.   l  Main  goal  of  insulin  therapy  is  to  fix  the  acidosis.   18  
  19. 19. Transitioning  to  Subcutaneous  Insulin   l   ONLY  after  the  Anion  Gap  is  closed!   l  OVERLAP  IV  and  subcutaneous  insulin  administration   l  Give  long-­‐acting  insulin  dose  (ex.  lantus)  at  least  30  to  60   minutes  prior  to  stopping  insulin  drip.   l   Feed  patient   19  
  20. 20. Managing  electrolytes   l  Potassium   l  Sodium   l  Phosphorus   l  Glucose   20  
  21. 21. Electrolyte  management   Potassium   Total  Body  Potassium  depletion   l  Acidosis    K+  exits  cells  as  H+  enters  to  buffer     l  Dehydration  and  volume  depletion   l  Osmotic  diuresis  +    aldosterone    loss  of  K+       Although  serum  K+  is  usually  normal  or  high,  total  body  K+   is  low.   21  
  22. 22. Electrolyte  Management   Potassium   l  With  insulin  therapy   l  K+    moves  into  cells   l  To  avoid  hypokalemia   l  Give  oral  and/or  IV  potassium  to  avoid  hypokalemia  when  K   <  4.5   l  Monitor  K+  levels  and  EKG     l  Low  K  –  Biphasic  T,  U-­‐wave   l  High  K  -­‐  tall  peaked  T,  flat  P  waves,  wide  QRS   l  Cardiac  dysrhythmia   22  
  23. 23. Electrolyte  Management   Sodium   Pseudohyponatremia:   l  For  each  100mg/dl  increase  of  glucose  above  100,          Na+  decreases  by  1.6  mEq/L     l  Corrected  Na+  =  measured  Na  +                                                      1.6  meq/L  x  (glucose-­‐100)/100))   l  Example:   Na+  =  125  meq/L  and  Glucose  =  500  mg/dl   500  –  100  =  400   400/100    =  4   4  x  1.6  =  6.4  meq/L     Corrected  Na+  =  125  +  6.4  =  131.4  meq/L   23  
  24. 24. **Electrolyte  Management   Phosphorus   Hypophosphatemia   l  Occurs  after  aggressive  hydration/treatment   l  Monitor  phosphorus  and  replete  as  needed  to  keep  >  1   l  Total  body  phosphorus  depleted   l  Mostly  a  theoretical  problem   l  Potential  complications:  muscle  weakness,  myocardial   dysfunction,  CNS  depression   24  
  25. 25. Management  review   l  Rehydrate  patient  with  IV  fluids   l  Continue  insulin  drip  until  anion  gap  is  closed   l  Until  insulin  drip  is  off:   l  Check  glucose  every  hour.  Avoid  hypoglycemia.   l  Check  electrolytes  every  1-­‐2hrs.  Avoid  hypokalemia.   l  Replete  potassium  when  K  <  4.5  and  patient  making  urine     25  
  26. 26. ICU  Monitoring   Careful  nursing  monitoring  of  the  following:   l  I/Os  (input  and  urine  output.)   l  Urine  dipstick  with  every  void   l  resolution  of  ketonuria  may  lag  behind  clinical  improvement   l  Monitor  for  any  signs  of  cerebral  edema:   l  Change  in  mental  status,  severe  headache   l  Sudden  drop  in  heart  rate   l  Neurologic  deficits     26  
  27. 27. DKA  Complications   l  l  l  l  l  l  l  l  l  Dehydration,  shock,  hypotension     Hypokalemia/  hyperkalemia   Hypoglycemia     Aspiration  pneumonia   Sepsis   Acute  tubular  necrosis   Myocardial  infarction   Stroke   Cerebral  edema     *    Death  rate  in  U.S  when  managed  in  hospital  setting          =  1-­‐4%   27  
  28. 28. DKA  Complications   Cerebral  edema   l  Clinical  manifestations:   l  Altered  mental  status   l  Headache   l  Persistent  vomiting   l  Sudden  and  persistent  drop  in  heart  rate   l  Seizure   l  Unequal  or  fixed,  dilated  pupils   l  Mostly  children   l  High  mortality  rate   l  1%  of  DKA  pts,  >  25%  mortality  rate   l  High  morbidity  rate   l  High  rate  of  neurologic  complications   28  
  29. 29. DKA  Complications    Cerebral  edema   l  Risk  Factors   l  Age  <  5  years   l  More  often  seen  in  your  sickest  patients     l  (high  BUN,  low  bicarb  <15)   l  Fall  in  serum  Na  or  lack  of  increase  during  treatment   l  Rapid  correction  of  hyperglycemia   l  Goal:  decrease  glucose  <100  mg/dl  (5.5)  per  hour   l  Sodium  bicarbonate  administration   l  Excessive  fluids   29  
  30. 30. DKA  Complications   Cerebral  Edema  -­‐  treatment   l  Mannitol  1mg/kg  IV   l  Reduce  IV  fluid  rate    (ex.  70%  maintenance)     l  Consider  intubation   l  set  the  ventilator  close  to  rate  that  patient  was  breathing   beforehand   l  be  cautious  of  over  hyperventilation   l  Temporary  measure   l  Keep  pCO2  >  22mmHg   l  May  consider  3%  hypertonic  saline   l  but  not  enough  data  to  truly  recommend   30  
  31. 31. Diabetic   HHS   Definitions    -­‐  Hyperosmolar     Ketoacidosis   hyperglycemic  state)     (AKA  HONKC  =      hyperosmolar  nonketotic  coma)   Blood  glucose   Glucose  >250  (13.9)   Glucose  >600  (33.3)   Arterial  pH   pH  <7.3   pH  >7.3   Serum  Bicarbonate   <15   >15   Serum  osmolality   varies   >320  mOsm   Urine  ketones   +++   small   Anion  gap   >12   Demographics   Mostly  type  I  DM   Children,  young  people   Mostly  type  II  DM   Elderly   Insulin  activity   Absolute  functional   insulin  deficiency   Relative  insulin  deficiency   Mortality  in  admitted   patients   1-­‐4%   10%  or  more   31  
  32. 32. HHS   (Hyperosmolar  Hyperglycemic  State)   l  Elderly  and  mentally  or  physically  impaired  patients   l  Usually  associated  with  underlying  physiologic  stressors   l  Ex.  Infection,  myocardial  infarction,  stroke.     l  Slower  onset  (ex.  1  week  vs.  1-­‐2  days  in  DKA)   l  Higher  Mortality  rate  than  DKA  (>10%)   l  Older  patients,  more  comorbidities   Presentation:   l  Altered  mental  status  (confusion,  neurologic  deficits)   l  Signs  of  severe  dehydration  (tachycardia,  hypotension,  dry   mucous  membranes,  skin  tenting)   32  
  33. 33. Insulin  Deficiency   Glucose  uptake   Lipolysis   Proteolysis   Glycerol   Free  Fatty  Acids   Amino  Acids   Hyperglycemia   Gluconeogenesis   Glycogenolysis   Ketogenesis   Osmotic  diuresis   Dehydration   Acidosis   ² No  Liploysis  =  No  Ketoacidosis   ² Only a small amount of functional insulin required to suppress lipolysis   ² Low  catecholamine  levels  in  elderly  patients  à  less  insulin  resistance   33  
  34. 34. HHS    -­‐  State  of  severe  dehydration   Therapy:   l  Fluid  repletion   l  Total  fluid  deficit  ≈  10  liters  in  adults   l  Normal  saline  2-­‐3  liters  rapidly   l  Replete  ½  in  first  6  hours   l  Insulin  drip  0.05  units/kg/hr   l  Decrease  glucose  by  approximately  50  mEQ/hr   l  Check  electrolytes  q1-­‐2hrs.  Check  glucose  q1hr   l  Monitor  potassium  for  hypokalemia/hyperkalemia   •  Treat  underlying  precipitating  illness     •  Potential  complications  are  the  same  as  DKA     34  
  35. 35. Summary   l  Pathophysiologic  difference  between  DKA  and  HHS   l  DKA  is  a  state  of  absolute  functional  insulin  deficiency   l  Only  in  DKA  :  Lipolysis  ketogenesis  acidosis     l  You  are  never  specifically  treating  the  glucose   l  In  DKA  –  you  are  treating  the  underlying  acidosis/ ketogenesis  (reflected  by  the  anion  gap)   l  In  HHS  –  you  are  treating  the  underlying  shock  caused  by   poor  tissue  perfusion/severe  dehydration   35  
  36. 36. Summary  (continued)   l  Being  too  aggressive  in  management  may  cause  more   harm  than  good   l  If  you  don’t  pay  attention  to  details,  you  will  cause  an   iatrogenic  death   l  Monitor  electrolytes  (especially  potassium)   l  Beware  cerebral  edema.   l  Therapy  for  DKA  and  HHS  is  similar.   36  
  37. 37. Thank  you   diabetees.spreadshirt.com   37  
  38. 38. Pathophysiology of diabetic ketoacidosis Source  Undetermined   38  
  39. 39. Islets  of     Langerhans   Stress   β-­‐cell  destruction   Polyuria   Volume  Depletion   Ketonuria   Decreased  Glucose  Utilization  &   Increased  Production   isol   Epi,Cort GH   Amino   Acids   Increased  Lipolysis   Insulin  Deficiency   Muscle   Increased  Protein     Catabolism   FattyAcids   Threshold   180  mg/dl   39   Glucagon   Liver   Increased  Ketogenesis,   Gluconeogenesis,   Glycogenolysis   Hyperglycemia   Ketoacidosis   HyperTG  
  40. 40. Additional  Information   Attributions  for  Slide  39:   Islets  of  Langerhans:  Afferent  (WikimediaCommons)   Adipocytes:  DBCLS  (WikimediaCommons)   Muscle:  Jeremy  Kemp  (WikimediaCommons)   Liver:  Mikael  Haggstrom  (WikimediaCommons)   Kidney:  Holly  Fischer  (WikimediaCommons)   40  

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