GEMC- Diabetic Emergencies- Resident Training
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GEMC- Diabetic Emergencies- Resident Training

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This is a lecture by Dr. Andrew Wong from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the ...

This is a lecture by Dr. Andrew Wong 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 Emergencies- Resident Training GEMC- Diabetic Emergencies- Resident Training Presentation Transcript

  • Project: Ghana Emergency Medicine Collaborative Document Title: Diabetic Emergencies Author(s): Andrew Wong (University of Michigan/St. Joseph Mercy Hospital), MD 2012 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
  • 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. 2 To use this content you should do your own independent analysis to determine whether or not your use will be Fair.
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  • Objectives —  Pathophysiology  of  diabetes   —  Signs,  symptoms,  diagnosis  and  management  of  acute   complications  of  diabetes:   —  Hypoglycemia   —  Diabetic  ketoacidosis   —  Hyperglycemic  hyperosmolar  nonketotic  coma 4
  • Case  1 —  23yo  F  with  history  of  DM  Type  I  presents  to  the  ED  for  difficulty   breathing.   —  7  days  ago,  she  began  having  vaginal  spotting,  and  dysuria   —  She  lost  her  glucometer  earlier  this  week  and  was  unable  to   measure  blood  sugars   —  Today,  she  began  to  have  nausea  and  vomiting  and  complained   of  abdominal  pain.       —  Mother  also  noticed  that  she  was  having  a  hard  time  breathing   —  Found  glucometer  today  and  it  read  “high” 5
  • Case  1 —  PMH:  Type  I  DM   —  PSH:  None   —  Medications:  Cannot  recall—uses  both  short  acting  and   long-­‐acting  insulin   —  Allergies:  None   —  SH:  Sexually  active;  denies  any  illicit  drug,  alcohol  or   tobacco  use.    Senior  in  high  school   6
  • Case  1 —  Physical  Exam:   —  VS:  T37  BP100/70  HR120  RR38  O2sat100%ra   —  General:  ill-­‐looking  thin  female  who  appears  to  have  labored   respirations   —  HEENT:  PERRL,  EOMI,  MM  dry,  OP  clear   —  Neck:  soft,  supple  with  no  lymphadenopathy   —  Lungs:  CTAB,  no  w/r/r   —  CV:  tachycardic  but  regular  rhythm,  no  m/r/r   —  Abdomen:  +BS.    Diffusely  tender  with  area  of  maximal  tenderness   in  the  LLQ.    No  lesions  found.    No  adnexal  masses  palpated   —  Pelvic:  White  creamy  exhudate  with  +CMT  and  left  adnexal   tenderness   —  Extremities:  cool  to  touch.    2+  radial,  DP  and  posterior  tibial  pulses   cap  refill  3  seconds.   —  Skin:  No  rash,  +skin  tenting   7
  • Normal  Physiology —  Glucose  rise  triggers  pancreatic  beta  cells  to  release  insulin   —  Insulin  lowers  serum  glucose  levels   —  Stimulate  glucose  uptake  and  storage,  facilitate  use  by  fat  and   muscle   —  Inhibit  glycogen  breakdown  in  liver   —  Degraded  in  3-­‐10  min  in  liver  and  kidney   —  Inhibits  hepatic  gluconeogenesis  and  glycogenolysis   —  Stimulate  glycogen  (stored  form  of  glucose)  storage   —  Fasting  state  stimulates  pancreatic  alpha  cells  to  release   glucagon   —  Glucagon  increases  levels  of  glucose  in  blood   —  Stimulate  liver  to  break  down  glycogen  and  release  glucose   —  Kidney  release  glucose  in  prolonged  starvation   —  Increases  ketone  production  to  enhance  gluconeogenesis   8
  • Background —  Diabetes   —  Most  common  endocrine  disease   —  Spectrum  of  disorders    characterized  by  hyperglycemia  and   disturbances  in  carbohydrate  and  lipid  metabolism   —  Four  types  of  Diabetes   —  —  —  —  Type  I:  Immune-­‐mediated  or  idiopathic  failure  to  produce  insulin   Type  II:  Hyperinsulinemic  state  due  to  resistance  to  insulin   Gestational  Diabetes  Mellitis:  during  pregnancy;  similar  to  DMII     Impaired  Glucose  Tolerance:  increased  risk  of  developing  DMII   9
  • Epidemiology —  Prevalence  of  DM  in  US  is  6.6%   —  5-­‐10%  have  Type  I   —  90-­‐95%  have  Type  II   —  Groups  at  risk  for  DM   —  More  in  whites  than  nonwhites   —  Native  Americans   —  Age  of  onset   —  Peak  age  of  onset  of  Type  I  DM  is  10-­‐14years   —  Onset  of    Type  II  DM  tend  to  be  older;  younger  people   getting  disease  due  to  obesity   10
  • Clinical  Features Clinical  Features Type  I  Diabetes Type  II  Diabetes Body  habitus Lean Obese Age Younger  than  40yo Middle-­‐aged  or  older Insulin  levels Absent  or  low Normal  to  high Onset Abrupt Gradual —  Initial  presentation  of  Type  I  DM  usually  DKA   —  Type  II  DM  is  being  Dx  in  younger  people   —  Diagnosis:   —  Any  random  plasma  glucose  >200mg/dL  (11.1  mmol/dL)  with  symptoms  of  diabetes   —  Fasting  plasma  glucose  >126mg/dL  (7mmol/dL)   —  Plasma  glucose  >200mg/dL  (11.1  mmol/dL)  on  2  hour  oral  glucose  tolerance  test. 11
  • Hypoglycemia —  Background   —  —  Below  70  mg/dL  (3.8mmol/ dL),  most  symptomatic   Precipitants:   —  —  —  —  —  —  —  —  —  —  —  —  —  —  Addison’s  disease   Akee  fruit   Anorexia  nervosa   Antimalarials   Decrease  in  usual  food   intake   Ethanol   Factitious  hypoglycemia   Hepatic  impairment   Hyperthyroidism   Hypothyroidism   Increase  in  usual  exercise   Insulin   Islet  cell  tumors   Malfunctioning,  improperly   —  —  —  —  —  —  —  —  —  —  —  —  adjusted,  or  incorrectly  used   insulin  pump   Malnutrution   Old  age   Oral  hypoglycemics   Overaggressive  treatment  of   DKA  or  HHNC   Pentamidine   Phenylbutazone   Propranolol   Recent  change  of  dose  or   type  of  unsulin  or  oral   hypoglycemic   Salicylates    Sepsis   Some  antibacterial   sulfonylureas   Worsening  Renal   Insufficiency   12
  • Hypoglycemia —  Background  (cont’d)   —  Hypoglycemia  unawareness   —  Somogyi  phenomenon   —  Signs  and  Symptoms   —  Secondary  to  secretion  of  epinephrine  and  CNS  dysfunction   —  Sweating,  nervousness,  tremor,  tachycardia,  hunger,  bizarre   behavior,  confusion,  seizures,  and  coma.   —  Diagnostic  Strategies   —  Obtain  blood  glucose  and  other  tests  to  find  cause   —  Factitious  hypoglycemia:  testing  for  insulin  antibodies  and  C   peptide  level   13
  • Oral  hypoglycemic  agents —  Non  hypoglycemic  (taken  individually)   —  Biguanides  (metformin)   —  decreases  hepatic  glucose  production   —  Alpha-­‐Glucosidase  inhibitors  (acarbose,  pioglitazone)   —  Decrease  GI  tract  absorption  of  glucose   —  Thiazolidinediones  (rosiglitazone,  pioglitazone)   —  Increase  peripheral  tissue  glucose  use   —  Hypoglycemic   —  —  Insulin   Sulfonylurea  (i.e.  glipizide)   —  Increases  pancreatic  insulin  secretion   —  Nonsulfonylurea  secretagogues  (repaglinide,  nateglinide)   —  Increased  pancreatic  insulin  secretion   —  Glucagon-­‐like  peptide  (Exanatide)   OsamaK,  Wikimedia  Commons     —  Stimulates  release  of  insulin  from  pancreatic  cells   —  Dipeptidyl  peptidase-­‐4  inhibitors   —  Inhibits  DPP-­‐4  to  prevent  degredation  of  endogenous  GLP 14
  • Hypoglycemia —  Management   —  If  patient  is  awake  and  cooperative,  give  sugar  containing  food   or  beverage  PO   —  If  unable  to  take  PO   —  25-­‐75  gm  glucose  as  D50W  (1-­‐3  amps)  IV   —  Children:  0.5-­‐1  g/kg  glucose  as  D25W  (2-­‐4mL/kg)   —  Neonates:  0.5-­‐1  g/kg  glucose  (5-­‐10mL/kg)  as  D10W   —  If  unable  to  obtain  IV  access:   —  1-­‐2  mg  glucagon  IM  or  SQ;  may  repeat  20  min   Intropin,  Wikimedia  Commons   15
  • Diabetic  Ketoacidosis —  Pathophysiology   —  Caused  by  cessation  of  insulin  intake  or  by  physical   emotional  stress   Source  undetermined   16
  • Diabetic  Ketoacidosis —  Clinical  Features   —  History   —  c/o  polydipsia,  polyuria,  polyphagia,  visual  blurring,  weakness,   weight  loss,  nausea,  vomiting,  and  abdominal  pain.   —  Seek  reason  for    DKA   —  Physical   —  —  —  —  Altered  mental  status   Tachypnea  with  Kussmaul  respirations   Hypotension  and  other  signs  of  dehydration   Acetone  breath   17
  • Diabetic  Ketoacidosis —  Diagnostic  Strategies   —  Laboratory  Tests   —  Glucose:  >350  mg/dL  (19.4  mmol/dL)   —  Euglycemic  DKA:  18%  pts  may  have  glucose  less  than  300  (16.6  mmol/ dL)   —  Sodium:  Low  to  normal   —  Correct  for  hyperglycemia:  0.016  x  (Glucose  -­‐100)   —  High  lipid  content  may  cause  falsely  low  levels.   —  Potassium:  Normal  to  high   —  Technically,  potassium  deficit  due  to  K+  and  H+  shifts   —  Correct  potassium  for  pH   —  (Serum  potassium)-­‐[0.6  (7.4-­‐pH)  x  10]   —  Acetoacetate  and  beta-­‐hydroxybutyrate:  elevated   —  BUN  and  Cr:  elevated   18
  • Diabetic  Ketoacidosis —  Management   —  ABCs,  IV,  O2,  Monitor   —  Blood  glucose,  labs   —  Dehydration   —  Fluids  mainstay  of  therapy;  pts  usually  down  3-­‐5L   —  Adult:  1-­‐2L  over  1-­‐3  hrs;  Child:  20  mL/kg  over  1  hour   —  Follow  with  fluid  resuscitation  to  maintain  UOP  of  1-­‐2mL/kg/hr   —  Insulin   —  Infusion  of  0.1  units/kg/hr  up  to  5-­‐10  units/kg/hr   —  Bolus  of  insulin  prior  to  drip  optional  in  adults;  contraindicated  in   children   —  Check  glucose  every  1  hour   —  Switch  IV  fluids  to  contain  dextrose  to  prevent  hypoglycemia  when   BS  250-­‐300  mg/dL  (13.8-­‐16.7  mmol/dL)   19
  • Diabetic  Ketoacidosis —  Correct  electrolyte  abnormalities  (check  basic,  pH,   ketones  every  2  hours)   —  Potassium   —  <4:  20mEq/hr   —  4-­‐6:  10mEq/hr   —  >6:  none   —  Magnesium   —  Supplement  0.30  to  0.35  mEq/kg/day  of  magnesium  if  deficient   (1-­‐3  grams  in  70kg  pt)   20
  • Diabetic  Ketoacidosis —  Acidosis   —  Bicarbonate  may  be  indicated  in  pts  pH  ≤  7.0   —  Usually  not  warranted   —  Worsen  O2  release  by  shifting  oxygen  dissociation  curve  to  left     —  Acidosis  correction  terminates  Kussmaul  respirations  needed  to   get  rid  of  CO2   —  Increases  K+  requirement   —  May  produce  alkalosis  which  induces  dysrhythmias  because  of   electrolyte  shifts   —  Inhibit  feedback  mechanism  in  which  low  pH  inhibits   ketogenesis   —  Studies  show  bicarbonate  worsens  prognosis  in  pts  even  with   pH  as  low  as  6.9-­‐7.1 21
  • Diabetic  Ketoacidosis —  Complications   —  —  —  —  —  Hypokalemia   Hypoglycemia   Alkalosis  (from  bicarb  therapy)   CHF   Cerebral  edema   —  Occurs  6-­‐10  hrs  after  initiation  of  therapy  and  unless  if  glucose  is   below  250mg/dL  (13.8  mmol/dL)   —  Consider  if  pt  remains  comatose  or  lapses  into  coma   —  Mortality  90%   —  Use  Mannitol  0.25-­‐2  mg/kg 22
  • Diabetic  Ketoacidosis —  Disposition   —  Admit  to  hospital/ICU   —  Consider  outpatient  if   —  —  —  —  —  Initial  pH>7.35   Initial  HCO3  ≥  20  mEq/L   Can  tolerate  PO  fluids   Symptoms  resolve  in  ED   No  underlying  precipitant  requiring  hospitalization 23
  • Hyperglycemic  Hyperosmolar   Nonketotic  Coma  (HHNC) —  Background   —  Characterized  by  hyperglycemia  (38.8),  hyperosmolarity,   dehydration,  and  altered  mental  status   —  Ketosis  and  acidosis  are  minimal  or  absent   Source  undetermined   24
  • HHNC —  Pathophysiology   —  Similar  to  DKA   —  Absence  of  ketoacidosis  is  unknown   —  Theory:  patients  continue  to  secrete  insulin  to   block  ketogenesis.   —  Etiology   —  More  common  in  type  II  DM   —  May  occur  in  non  diabetic  pts  (20%  of  cases)   especially  after  burns,  hyperalimentation,   peritoneal  dialysis,  or  hemodialysis Виталий  Поспелов,  Wikimedia  Commons   25
  • HHNC —  Clinical  Features   —  History   —  Fever,  thirst,  polyuria,  or  oliguria   —  Associated  with  chronic  renal  insufficiency,  gram-­‐negative  PNA,  GI   bleeding,  gram-­‐negative  sepsis.   —  Physical  Exam   —  —  —  —  —  —  —  hypotension  and  other  signs  of  dehydration   Tachycardia   Fever   Altered  mental  status   Seizures   Signs  of  stroke   Less  commonly:  choreoathetosis,  ballismus,  dysphagia,  segmental   myoclonus,  hemiparesis,  hemianopsia,  central  hyperpyrexia,   nystagmus,  visual  hallucinations,  and  acute  quadriplegia   26
  • HHNC —  Diagnostic  strategies   —  Laboratory  Testing   —  Blood  glucose  >600  mg/dL  (33.3  mmol/dL)   —  Serum  osmolarity  >  350  mOsm/L   —  May  have  metabolic  acidosis  2/2  lactic  acidosis,  starvation   ketosis   —  Electrolytes:  decreased  sodium,  elevated  potassium   27
  • HHNC —  Management   —  Dehydration   —  Usually  9L  fluid  deficit  in  a  70  kg  pt   —  2-­‐3L  of  NS  initially;  may  change  to  0.45%NS  afterwards   —  Sterile  water  to  be  considered  concommitently  for  pts  with  CHF   —  Insulin   —  Electrolytes   28
  • Case  1 —  Work-­‐up 29
  • Case  1 —  Laboratory  results:   Phos  7.3   Na  134   WBC  6.2   K  7.0   Hbg  3.6   Cl  106   Hct  9.9   HCO3  3   Plt  310   BuN  16   VBG  pH  7.2   Cr  1.4   Wet  Smear:  +  for  clue  cells   Glucose  770  (42.7)   Urine  Dip:  +LE,  Nitrite   Ca  9.4   Urine  Micro  15-­‐30wbc/hpf   Mg  2.6   30
  • Case  1 —  EKG:  Sinus  tachycardia  with  normal  axis,  intervals.     +Peaked  T  waves  in  leads  V1-­‐6   —  CXR:  no  infiltrates   —  Pelvic  Ultrasound:  no  acute  abnormalities.   31
  • Case  1 —  Hospital  course   —  Started  on  IV  fluids,  Insulin  drip   —  Started  on  Flagyl,  Cefotetan,  Doxycycline   —  Blood  and  urine  cultures  were  positive  for  E.  coli 32
  • Sources Marx  J.    Rosen’s  Emergency  Medicine,  7th  Ed,  2009.   Rucker  D.  “Diabetic  Ketoacidosis.”  eMedicine  Emergency   Medicine,  4  Jun  2010.   33