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/

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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

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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”

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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  

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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  

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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  

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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  

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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  

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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.

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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  

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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  

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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)  

�  Stimulates  release  of  insulin  from  pancreatic  cells  �  Dipeptidyl  peptidase-­‐4  inhibitors  

�  Inhibits  DPP-­‐4  to  prevent  degredation  of  endogenous  GLP

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OsamaK,  Wikimedia  Commons    

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  

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Intropin,  Wikimedia  Commons  

Diabetic  Ketoacidosis �  Pathophysiology  

�  Caused  by  cessation  of  insulin  intake  or  by  physical  emotional  stress  

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Source  undetermined  

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  

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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  

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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)  

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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)  

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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

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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

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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

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Hyperglycemic  Hyperosmolar  Nonketotic  Coma  (HHNC)

�  Background  �  Characterized  by  hyperglycemia  (38.8),  hyperosmolarity,  

dehydration,  and  altered  mental  status  �  Ketosis  and  acidosis  are  minimal  or  absent  

24 Source  undetermined  

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

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Виталий  Поспелов,  Wikimedia  Commons  

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  

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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  

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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  

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Case  1 �  Work-­‐up

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Case  1 �  Laboratory  results:  

Na  134  

K  7.0  

Cl  106  

HCO3  3  

BuN  16  

Cr  1.4  

Glucose  770  (42.7)  

Ca  9.4  

Mg  2.6  

Phos  7.3  

WBC  6.2  

Hbg  3.6  

Hct  9.9  

Plt  310  

VBG  pH  7.2  

Wet  Smear:  +  for  clue  cells  

Urine  Dip:  +LE,  Nitrite  

Urine  Micro  15-­‐30wbc/hpf  

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Case  1 �  EKG:  Sinus  tachycardia  with  normal  axis,  intervals.    

+Peaked  T  waves  in  leads  V1-­‐6  

�  CXR:  no  infiltrates  

�  Pelvic  Ultrasound:  no  acute  abnormalities.  

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Case  1 �  Hospital  course  

�  Started  on  IV  fluids,  Insulin  drip  �  Started  on  Flagyl,  Cefotetan,  Doxycycline  �  Blood  and  urine  cultures  were  positive  for  E.  coli

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Sources Marx  J.    Rosen’s  Emergency  Medicine,  7th  Ed,  2009.  

Rucker  D.  “Diabetic  Ketoacidosis.”  eMedicine  Emergency  Medicine,  4  Jun  2010.  

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