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Diabetic Emergencies

Diabetic Emergencies. Caroline Kowal January 22, 2004. Objectives. DKA HONK Hypoglycemia. Diabetic Ketoacidosis. 8-28% of all DM admissions 20-30% cases in new onset DM Body’s response to cellular starvation

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Diabetic Emergencies

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  1. Diabetic Emergencies Caroline Kowal January 22, 2004

  2. Objectives • DKA • HONK • Hypoglycemia

  3. Diabetic Ketoacidosis • 8-28% of all DM admissions • 20-30% cases in new onset DM • Body’s response to cellular starvation • Insulin deficiency, excess counterregulatory hormones (glucagon, catecholamines, cortisol, GH)

  4. DKA Pathophysiology • Relative insulin deficiency • Decrease glucose utilization • Breakdown glycogen = increase glucose • -------------------------- • Breakdown protein – gluconeogenesis • Not using glucose • Making more glucose – Hyperglycemia • Osmotic diuresis

  5. Pathogenesis DKA

  6. Osmotic Diuresis • Cause manifestations of DKA (volume loss) • Will continue to lose glucose through the urine (20g/d glucose can be lost) • Serum glucose will not continue to rise in the serum. Homeostatsis will occur • If pt drinks, the diuresis will continue. Cannot drink enough to keep up

  7. Insufficient insulin – get free fatty acid breakdown • Free fatty acids contribute to gluconeogensis and Ketogenesis • Ketones cause nausea,vomitting,anorexia, ileus • Pt unable to drink secondary to anorexia, so glucose continues to rise rapidly, diuresis continues, pt crashes

  8. As osmolarity increases affects the LOC • Renal failure will go into DKA rapidly • Loss Cl < K

  9. ADA Diagnostic Criteria DKA and HHSMild Mod Severe HHS Plasma glucose (mmol/l) >13 >13 >13 >33 Arterial pH7.25–7.30 7.00–7.24 <7.00 >7.30 Serum bicarbonate (mEq/l)15–18 10 to <15 <10 >15 Urine ketones + + + + Small Serum ketones + + + small Effective serum osmolality (mOsm/kg) Variable Variable Variable >320 Anion gap >10 >12 >12 <12 Mental obtundationAlert Alert/drowsy Stupor/coma Stupor/coma

  10. Clinical Presentation DKARelated to 3 metabolic derangements • Hyperglycemia • Increased osmotic load, diuresis • Renal losses Na, Cl, K, PO4, Ca, Mg • Polyuria, polydypsia, 2. Volume depletion • Poor absorption of sc insulin 3. Acidosis • Compensatory tachypnea to decrease PCO2 and counter metabolic acidosis • Causes profound vasodilation • N/V/abdo pain from ketones Decreased LOC/Coma related to osmolarity, usu serum osmolarity >340mOsm/L.

  11. Typical total body deficits of water and electrolytes in DKA and HHS • Total water (l) 6 9 • Water (ml/kg) 100 100–200 • Na+ (mEq/kg) 7–10 5–13 • Cl- (mEq/kg) 3–5 5–15 • K+ (mEq/kg) 3–5 4–6 • PO4 (mmol/kg) 5–7 3–7 • Mg++ (mEq/kg) 1–2 1–2 • Ca++ (mEq/kg) 1–2 1–2

  12. Is this really DKA? • Hyperglycemia NOT predominant factor • As in having a very high serum glucose • >13mmol/L • Can have euglycemic DKA • Acidosis pH < 7.3, HCO3 < 18 • Increased anion gap • Ketonuria (3+ or 4+) sensitive but not specific • or ketonemia

  13. Spectrum of DKA • DM type I or II • Type II usu are young, obese, not yet diagnosed diabetics • ++ high relative insulin insufficiency • Takes hours to days to get into DKA • Tachycardic (increased minute ventilation) • Acetone breath

  14. Evolves over 24h N/V/Abdo pain Can have hemorraghic gastritis (coffee ground emesis) Tachycardia (increased minute ventilation) Mortality rate 5% Evolves over hours to days Usually no abdo pain Pts usu much older Greater hyperglycemia and volume contraction Greater hyperosmolarity with resultant prominent mental status changes Little to no anion gap metabolic acidosis Mortality rate 15-30% DKA vs. HONK

  15. DDx DKA DDx for AG Metabolic acidosis (MUDPILES) M = methanol U = uremia D = DKA and AKA P = paraldehyde, propylene glycol I = INH, iron L = lactate E = ethylene glycol, ethanol S = salicylate, starvation

  16. Precipitants of DKA • Infection 1/3 • UTI, pneumonia, sepsis, pilonidal abcess, perianal abcess • Noncompliance 1/3 • Frequent with pt who cannot afford insulin • New Onset • MI, CVA, PE • Surgery, steroid use, pregnancy • Insulin pump patients with pump failure • Can go into DKA in hours

  17. Standardized intervention protocols have been shown to decrease mortality in DKA

  18. Initial Workup • Accucheck • Blood/urine glucose • Venous gas • CBC, Electrolytes, BUN, Cr, Ca, PO4 • Urinalysis • Cultures, ECG, CXR

  19. Acidosis + HyperglycemiaUsu AG metabolic acidosis • Does not necessarily mean you are in DKA • Pregnant pt and EtoH usu do not have impressively high glucose levels • Many medicolegal cases on this • Pt may actually be sepsic and the acidosis is from lactate • Hyperchloremic acidosis – ketone exchange for Cl in urine. Usu in pt with good hydration. • Metabolic alkalosis – vomitting, osmotic diuresis, diuretic use • May have normal HCO levels with only clue to DKA being elevated AG

  20. No Need for ABG’sMa Oj et al.Acad Emerg Med 2003 Aug;10:836-41 • Strong correlation between arterial and venous gases in DKA • 200 pt with suspected DKA had both ABG and venous gases done within 30 min if each other • Values correlated well (venous values 0.015 units lower than ABG) • Results of ABG did NOT affect tx or disposition

  21. Nitroprusside Reagent • Ketones – acetoacetic acid (AcAc) and betahydroxybutyrate (BHB) • BHB is strongest and most prevalent acid in DKA • BHB is oxidized to AcAc (usu 3:1 ratio, in DKA is a 12:1) • Nitroprusside reagent detects only AcAc to detect urine and serum ketones • Ketone levels will rise as pt is being tx (more BHB converted to AcAc) • May falsely lead you to believe that ketosis is worsening • Check ketones only once, if positive no need to repeat

  22. All pt will have an increased WBC (demarginalization) • If infection is precipitant may see a left shift • ABG helpful initially if you cannot get bloodwork STAT • Venous gas only 0.03 different (in sicker pts) • Anion gap (Na – Cl + HCO3) usu 10-12

  23. Spurious Hyponatremia • Corrected Na = • Measured Na + 1.6 X (glucose – 100) 100 American numbers – to use it take our glucose X 18 then plug into formula

  24. Treatment DKACorrect over 24 – 36 h • ABC’s • Fluid replacement # 1 • Volume deficit leads to serious manifesations DKA • Insulin • Will clear the ketones • Normalization of AG takes 8 -16h • K+ repletion • Treat precipitant

  25. Fluid Replacement • Adults ~10L deficit (100 ml/kg) • Start with NS • 1L over first 30 min then repeat. On average pt get 3L NS before switch to ½ NS. (Depends on serum Na) • 1st 2L over 0 – 2 h, next 2L over 2 – 6h, then 2L over 6 – 12h • ½ NS (14mg/kg/h) if corrected serum Na is normal or elevated • D5 ½ NS once glucose decreased but still need free water. Need more insulin to stop ketogenesis.

  26. Pediatric Fluid Therapy • Pediatrics 10 -20 cc/kg boluses, may be repeated • Do not exceed 50ml/kg bolus in first 4 hours • Change to ½ NS at 1.5X maitenance rate and run over 24h

  27. NS vs ½ NS • Not much data • Not known precisely when to switch • Pt with hyper/hypoNa have worse prognosis • Pt w Na in normal Na range, it doesn’t really matter when you switch to ½ NS

  28. Hemodynamics of pt most important • Once pt starts to produce urine • Intravascular volume replete • Intracelluar volume depleted (do this slowly) • Autonomic neuropathy may make HR less predictive of volume status • Follow urine output! • Tachycardia may be related to precipitating factors

  29. Fluids and insulin have same rate of recovery! • Insulin can be given iv or im • Insulin 0.1U/kg/h • No bolus in adults (no faster recovery with insulin bolus) • Bolus in kids (as per the ADA, no real evidence) • Insulin 1U/h has been attempted and in a case series of ~120 pts there have been no deaths • Infection is main cause of nonresponse to insulin. If no change in 1h double iv infusion insulin (0.2 – 0.4U/kg)

  30. Insulin binds to plastic in tubing • Need to flush tubing first • Flush ~ 50 ml • If do not flush, it make take 20 – 30 mintues for pt to actually get any insulin

  31. Resolution of hyperglycemia before ketones and acidosis • Continue insulin infusion until ketones and acidosis cleared (usu ~12h)

  32. Start SC insulin once pt drinking/eating • Overlap the sc and and iv insulin • iv insulin will last in body 5 – 7 minutes • NPH + Humulin • Sliding scale

  33. PotassiumHypokalemia can kill • Goal of K+ replacement is to keep normal levels extracellular K+ during acute phase, correct intracellular K+ over days • Insulin causes K+ shift intracellular (rapid hypokalemia can cause arrythmias, respiratory paralysis, paralytic ileus, rhabdomyolysis)

  34. Goal serum K+ = 4–5 mEq/l • K+ < 3.5mEq/L: replace with 40mEq KCl/L • K+ 3.5 – 5.5mEq/L: replace with 20 – 30mEq/l • K+ >5.5mEq/l – Hold K+ • Start insulin 30 minute after you replace K+ if initally < 3.5 (get K+ >3.3mEq/l first) • KPO4 and KCl replacement are equal

  35. PO4 • Not necessary to replace unless severely low • Can ppt hypo Ca, Hypo Mg • Wait until pt can eat, the PO4 will correct itself

  36. Pros Improved myocardial contractility Elevated vfib threshold Improved response to catecholamines Decreased work of breathing Cons Worsening hypokalemia Paradoxical CNS acidosis Worsening intracellular acidosis Impaired oxyHg dissociation curve Rebound alkalosis Hypertonicity Delayed recovery from ketosis (ketone body metabolism produces alkalis) BicarbGive only if pH <7.0 and give SLOWLY pH <7.0 and worsening ph despite aggressive management – think of other causes

  37. Bicarb • No studies showing bicarb to help or to cause furthur harm • ADA recommends: • Adult patients with a pH <6.9: • 100 mmol NaHCO3 be added to 400 ml sterile water and given at a rate of 200 ml/h. • pH of 6.9–7.0: • 50 mmol NHCO3 is diluted in 200 ml sterile water and infused at a rate of 200 ml/h. • No bicarbonate is necessary if pH is >7.0 • In peds if pH < 7.0 1–2 mEq/kg sodium bicarbonate over the course of 1 h

  38. Complications DKA 1. From disease • High mortality from sepsis and MI • Severe vol depletion increases risk DVT • Prophylatic heparin can be used in high risk in pts 2. Early complications related to therapy • Hypoglycemia, hypokalemia, hypoPO4, ARDS, cerebral edema, pulmonary edema 3. Late complications • Vascular thrombosis (cerebral vessels most susceptible)

  39. Cerebral Edemain 1% of all pediatric DKA’sNicole Glaser et al.Risk Factors for Cerebral Edema in Children with Diabetic Ketoacidosis. NEJM, Vol. 344, No. 4. Jan 25, 2001 • 15 year multicenter “control” study • 61/6977 children with DKA who developed cerebral edema • Pt with cerebral edema tended to be much sicker at baseline • CT/MRI studies show cerebral edema prior to treatment • Glaser found pt with cerebral edema had lower PCO2 and higher

  40. Hyperosmolar Hyperglycemic Non ketotic Syndrome (HHNK) • Definition: • Extreme hyperglycemia > 22mmol/L • Osmolality >315mosm/kg • Bicarbonate > 15 • pH > 7.3 • Serum negative for ketones in 2:1 dilution • Profound metabolic acidosis with mild ketones also seen (starvation ketosis)

  41. Why are pt not ketotic? • Lower levels of counterregulatory hormones (inhibits lipolysis) • Higher levels endogenous insulin (strongly inhibits lipolysis) • Inhibition of lipolysis by hyperosmolar state

  42. Presentation HHNKMisdiagnosis of stroke is common! • Usually elderly • Stuble changes in vital signs or mental status • Weakness, anorexia, fatigue • May present with focal or generalized seizures (resistant to anticonvulsants) • Tremor, clonus, hyper/hyporeflexia, + babinski, reversible hemiplegia or hemisensory deficits (without CVA or intracerebral lesions) • Undiagnosed or poorly controlled DM II • Limited access to free water (may have poor cognition or physical limitations)

  43. Infection UTI, pneumonia, viral illness Parenteral or enteral nutrition GI Bleed, pancreatitis PE Heat related illness Mesenteric ischemia Infection MI Severe burns Renal insufficiency Peritoneal or hemodialysis Stroke Rhabdomyolysis Seizures (15%) Precipitants HHNK

  44. Diuretics Lithium B blockers Calcium channel blockers Mannitol Steroids Neuroleptics Phenytoin Didanosine Drugs that can Preciptiate HHNK

  45. Labs • Additional to regular DKA labs consider: • LFT’s, lipase • Troponin • TSH • PT, PTT, INR • Lumbar puncture • CT head

  46. Treatment • 1. Correct hypovolemia • Fluid deficit 20 -25% TBW ( 8-12L) • In elderly 50% of body wt is TBW • Replace first ½ in 12h, remainder over next 24h • Change to ½ NS once hypotension, tachycardia and urine output improve • 2. Treat ppt • 3. Correct electrolyte abN • Use 2 iv’s with KCL. Some feel rapidly replacing K through central line poses risk for conduction abN • 4. Correct hyperglycemia

  47. Insulin • Be sure to correct volume contraction FIRST • If start insulin first will worsen dehydration (osmotically active glucose will shift intracelluar bringing water with it) • Correct hypokalemia prior to insulin therapy

  48. Hypoglycemia • Common in type I diabetics • Somogyi phenomenon • Iatrogenic hypoglycemia • Excessive insulin dosage unrecognized hypoglycemia in sleeping pt counterreg hormones cause hyperglycemia • Need to decrease dose insulin • S&S due to excessive epinephrine and CNS dysfxn: • Sweating, nervousness, tremor, tachycardia, hunger, neurologic sx (bizarre behaviour, confusion, sz, coma)

  49. Addison’s dz Anorexia nervosa Antimalarials Decrease po intake EtoH Facticious Hyper/hypothyroid Increase exercise Islet cell tumor Malfunctioning insulin pump Old age Oral hypoglycemia Too aggressive tx Pentamidine Propranolol Recent med change Salicylates Some sulfonylureas Worsening renal fxn Precipitants Hypoglycemia in Diabetics

  50. Tx Hypoglycemia in Diabetics • If pt awake and cooperative, eat or drink • If pt unable to take anything po: • 25-75g glucose as D50W (1-3 amps) iv • Peds: 0.5-1.0g/kg glucose as D25W iv (2-4ml/kg) • Neonates: 0.5-1.0g/kg (1-2ml/kg) as D10W • No iv: • 1-2mg glucagon im or sc, repeat q 20 min • Peds: 0.025-0.1mg/kg im or sc q 20 min

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