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DIABETIC EMERGENCIES

DIABETIC EMERGENCIES. Trevor Langhan MD January 31 st, 2008 University of Calgary. Objectives. Case based approach to important glucose related presentations Mixed in with some physiology to understand treatment plans. Case 1. 21 year old Japanese exchange student In Canada past 6 months

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DIABETIC EMERGENCIES

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  1. DIABETIC EMERGENCIES Trevor Langhan MD January 31st, 2008 University of Calgary

  2. Objectives • Case based approach to important glucose related presentations • Mixed in with some physiology to understand treatment plans

  3. Case 1 • 21 year old Japanese exchange student • In Canada past 6 months • Felt sick for past 2 days and was not eating • Now billeting family says he is acting confused

  4. Case 1 • In to ED via EMS • Pt too drowsy to provide accurate history • Responds to pain • Thin male, looks dehydrated • PMHx: Type 1 DM since 6 yrs old • Questions?

  5. Case 1 • Vitals: • T – 38.2 • HR – 130 • BP – 100/60 • RR – 28 • Sats – 98% • Bedside tests: • Chemstrip – “high” • Additional labs?

  6. Case 1 • Na+ 130 • K+ 6.3 • HCO 8 • Cl 108 • Cr 165 • Glucose 38 • What is his AG? • 14 – is this right?

  7. Na+ correction for increase Glucose • Multiple sources of information for formula…. • Common: • Increase Na+ 1.6 for every 5.6 mmol/L glucose • Easiest: • Increase Na+ 3 mmol/L for every 10 mmol/L of glucose

  8. Na+ correction for increase Glucose • Hyperglycemia (and hyperlipidemia) leads to increase in osmolar funciton of blood • H20 is drawn from the cells into the vascular space • Dilutional hyponatremia • For our guy his Na+ = 139 mmol/L • 3 mmol increase Na+ / 10 mmol glucose

  9. Case 1 • With the new Na+ his AG is actually 23 • So he has an anion gap metabolic acidosis…. • How are you going to get his acid/base status? • ABG vs. VBG…..

  10. Ma OJ et al. Arterial Blood Gas Results Rarely Influence Emergency Physician Management of Patients with Suspected Diabectic Ketoacidosis. Acad Emerg Med. Aug 2003, 10:8. • Prospective observational study • Inclusion: DKA pts • VBG, ABG, chem 6 • ABG result changed: • Altered treatment in 7/200 (3.5%, 1.7-7.1% CI) • dispostion in 2/200 cases (1%, 0.3-3.6% CI) • VBG pH correlated with ABG pH (r = 0.951)

  11. Case 1 • What is the source of his gap acidosis? • Ketone production from fatty acid breakdown • How are you going to prove that? • Urine vs. blood….

  12. Urine vs. blood • Urine dip stick • Nitroprusside reaction • Qualitatively assess for ketones • Only measures which ketone? • Acetoacetate • Does not measure B-Hydroxy Buterate • AA:BHB ratio is 1:3 (can be as high as 1:30) • So might have false –ve urine dip despite gross ketosis

  13. Case 1 • So you’ve proven he’s got an AGMA • And shown where the acidosis is coming from…. • Dx: Diabetic ketoacidosis

  14. DKA - Diagnosis • Clinical • Dehydration • High cap glucose • Ketones in urine or plasma • Confirmed: • Blood pH • Serum Bicarb • Serum Osmolality

  15. DKA • Three main problems: • Hyperglycemia • Osmotic diuresis • Dehydration – can be profound • 5-7 litre total fluid deficit • Loss of electrolytes • K+, Na+, Mg+, PO4- • Acidosis • Transcelluar shift of H+ and K+ • Falsely normal K+ (or even high)

  16. DKA - Treatment • Fluid rehydration • Pts in hypovolemic shock need assessment of ABCs • Treat with boluses of 0.9% NS • Avoid pressors – etiology of shock is decreased intravascular volume • Adults – 1-2 litres over 1 hour • Subsequent fluid change to 0.45% NS

  17. DKA- Treatment • Peds – 20 cc/kg bolus initially if shock • Otherwise start with 10 cc/kg • Goal to replace fluid deficit over 24-48 hours • Dreaded risk of cerebral edema….

  18. Multi-center, retrospective • Included DKA pts with CE • Matched for illness severity to DKA pts with no CE • Log regression • Risk Factors: • High urea • Use of Bicarb • Low PCO2

  19. Why do they get Cerebral Edema?

  20. Marcin JP et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. Journal of Pediatrics. 141(6); Dec 2002. • 3 variables were found to be associated with a poor outcome of children with DKA-related cerebral edema • Elevated initial BUN concentration • More profound neurologic depression at the time of diagnosis of cerebral edema • Intubation with associated hyperventilation to a PCO2 level <22 mm Hg.

  21. DKA - Treatment • Boluses of fluid to increase intravascular volume • What next? • Stop lipolysis and the production of ketone bodies • His glucose is 38 mmol/L • How do you want to treat him?

  22. DKA - Treatment • IV regular insulin is the start • No RCT to prove bolus vs. just starting an infusion • Current practice is to only start an infusion at 0.1 unit/kg/hour • No need to quickly drive glucose into the cells • Rehydration and osmotic diuresis will eliminate most excess glucose

  23. Umpierrez GE et al. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome. Am J Med Sci. 311(5); May 1996, pp 225-233. • Kitabchi et al. Compare ‘high dose’ to ‘low dose insulin’ in DKA treatment • RCT, prospective • No difference in: • Rate of decline of blood glucose • Rate of decline of ketone body concentration • Time to resolve acidosis • High doses of insulin associated with: • 25% increase in hypoglycemic events • Greater hypokalemia

  24. DKA - Treatment • Current standard has become ‘low dose’ insulin • Constant infusion at 0.1 units/kg • No current need to bolus administer insulin

  25. DKA - Treatment • As glucose is trending down add a glucose containing solution to IV fluid • Glucose < 14 mmol/L • Drop insulin infusion by 50% • Add D5 to your ½ NS maintenance • Run at 200-400 cc/hr for first 12 hours

  26. Loss of Electrolytes

  27. Electrolyte Replacement • Loss of: • Cl-, Na+, K+, PO4 • Most NB to replace is K+ • Myocardial cell membrane stability • Risk of dysrhythmia, death

  28. Electrolyte Replacement • DKA – K+ may be normal or elevated • Acidosis may lead to ‘false normal’ K+ levels • True body K+ much lower • Treatment of DKA may lead to lowering of K+ • Insulin • HCO3

  29. Electrolyte Replacement • Hold insulin until you’ve checked the K+ • Don’t give insulin if K+ < 3.3 mmol/L • If K+ normal or high start rehydration and insulin • K+ < 5.0 mmol add 20-40 mmol/L of K+ to IV fluids • Ensure Mg+ supplemented as well

  30. DKA – Treatment summary • IV fluids – bolus ++ if shocky • Check lytes • Replace K+ early • Add to IV fluid as K+ < 5.0 mmol/L • Insulin infusion 0.1 units/kg/hr • Look for inciting event… • Infection, MI, trauma, pancreatitis…

  31. DKA - Treatment • Bicarb is rarely indicated • Risk of hypokalemia • No proven indications • Guidelines suggest that if: • pH < 7.0 – after 1 hour of treatment • Give one amp diluted in 200 cc over 1 hour

  32. CASE 1-B • 77 y F from nursing home • Not eating or drinking lately • Vague abdominal pain expressed to care home staff yesterday • Didn’t come down for lunch

  33. CASE 1-B • EMS called when she was found in her room • HR 120 BP 90/50 RR 18 Sat 98% • GCS 9 • Glucose ‘high’

  34. CASE 1-B • Labs: • Na+ 144 mmol/L • K+ 5.4 mmol/L • Cl- 124 mmol/L • HCO3 20 mmol/L • Glucose 49 mmol/L • Urea 15 mmol/L • VBG 7.34 / 40 / 90 / 21

  35. Hyperosmolarity • 2 Na+ + gluc + urea = osmolarity • DKA osmo usually < 320 mmol/L • HHS > 320 mmol/L

  36. Hyperglycemic Hyperosmolar State • Formerly known as HONK • Pts can have ketosis so misleading name • Marked hyperglycemia and dehydration • Profound electrolyte losses • Due to insulin resistance and excess counter regulatory hormones

  37. Hyperglycemic Hyperosmolar State • More likely to occur in older, obese pts • More often Type 2 DM • May develop over days – weeks • Frequent in elderly: • free water deprived • compromised renal fxn

  38. Hyperglycemic Hyperosmolar State • Some insulin present so no ketone production • No subsequent acidosis (pH > 7.3)

  39. Hyperglycemic Hyperosmolar State • LOOK for underlying cause • Older more frail pts • IV fluids • Insulin infusion • Monitoring and correction of electrolytes • K+ depleted but not as low as DKA • No acidosis, so no shift

  40. Diagnosis - Laboratory

  41. Complications of DKA and HHS • Cerebral Edema • ARDS • Hypoglycemia and Hypokalemia • Thrombosis and PE • No RCT to tell us what to do • Venous stasis, viscous blood, underlying artherosclerosis – set up for clot • Consider Heparin sc for DVT prophylaxis in high risk patients

  42. Prognosis - summary • DKA mortality 4-10% • HHA mortality 10-50% • Not as different as I always thought: • IV fluids • Lower glucose with IV insulin infusion • Anticipate and correct electrolyte abnormalities (K+ most NB in DKA) • Add glucose to IV at gluc < 15 mmol/L • Look for precipitant

  43. CASE 2 • 3 month old boy with gastroenteritis • To ED with parents lethargic • Has not been eating well • Clinically looks dry • Glucose 1.6 mmol/L • Tx: 4 cc/kg D10W • IV fluids, improved

  44. CASE 3 • 25 y female • Took her insulin 30 minutes ago to kill self • Seizure in waiting room • Tx: IV glucose • 1 amp D50W • Additional amps as needed • May require infusion of D10W

  45. CASE 4 • 27 year old Type 1 DM • Took insulin this am as usual • Skipped breakfast, then vigorous exercise • Now confused, cant’ find keys • EMS called

  46. CASE 4 • Initial glucose 2.2 mmol/L • Vitals stable, GCS 13 • Given IM glucagon and some oral CHO • Now glucose is 6.6 mmol/L • Feels well, A&O x 3 • EMS patches to cancel transport • Alert, cooperative pts, responsible adults • Tolerating oral CHO

  47. Hypoglycemia - Summary • Bolus IV glucose • D50W adults (1-3 amps) • D25W peds (4 cc/kg) • D10W neonate-2 years (4 cc/kg) • NO IV can give Glucagon IM 1-2 mg • Prolonged hypoglycemia after OD of insulin may need Dextrose infusion D10W • Treatment is eating CHO meals

  48. CASE 5 • 55 year old male Type 2 DM • Acting confused at home • Wife called EMS • Meds: • Metformin • Altace • Glyburide • ASA

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