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Diabetic Emergencies

Diabetic Emergencies. March 19, 2009 Jennifer Hughes. Mr. H. 45 M with abdominal pain and feeling “unwell” x 10 days Presented to ED 1 week ago with abdominal pain, dx with Diabetes and started on Metformin. Pmhx: MI 1999 Labs at the time: 7.41/39/24 Na 122/K4.6/Cl 84/C02 18 Gluc 52

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Diabetic Emergencies

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  1. Diabetic Emergencies March 19, 2009 Jennifer Hughes

  2. Mr. H • 45 M with abdominal pain and feeling “unwell” x 10 days • Presented to ED 1 week ago with abdominal pain, dx with Diabetes and started on Metformin. • Pmhx: MI 1999 • Labs at the time: 7.41/39/24 • Na 122/K4.6/Cl 84/C02 18 • Gluc 52 • Urine ketones • Progressively worse over the week, polydipsia, polyuric, increasing pain

  3. Examination • Thin, cacectic • Appears unwell • Rapid breathing • Decreased LOC/mild confusion • BP 130/75, P 120, sats 95%, afebrile, RR 24. BG “high” • Abdomen diffusely tender, epigastrium ++, not peritoneal

  4. What do you do?

  5. Labs • 7.08/15/64/4 • HB 188, WBC 15, platelets 169 • BG 45 • Na 135, K 3.0, Cl 99 • EKG – sinus tach • Cr 129 • ALP 127, ALT 69, bili 7, GGT 68 • Lipase 2628 • Serum ketones small

  6. VENOUS blood gas • Winter’s formula • HC03 * 1.5 + 8 = pC02 (+/-2) • Indicates adequate compensation in metabolic acidosis

  7. D K A • pH < 7.3 • Bicarb < 15 mmol/L • AG > 12 • Serum / urine ketones • BG > 14 mmol/L Canadian Diabetic Association Guidelines 2008

  8. Are urine ketones good enough? • Uses a nitroprusside reaction • Good test for acetoacetate but NOT betahydroxybutyrate • DKA usually has a ratio acetoacetate/betahyroxybutyrate of 1:3 but it can be 1:30 • Rarely could have negative urine dip with very high ketonemia • Serum ketones = betahydroxybutyrate

  9. How do you want to manage this patient?

  10. DKA Management • ABCs but… • Try not to intubate these patients • Fluids • Potassium • Insulin • Look for underlying cause

  11. Fluids • Most important therapy • Reduces glucose by dilution and osmotic diuresis • Can give PO fluids • 1-2 L NS at beginning • Once euvolemic and if Na is normal/high – change to ½ NS • Once BG < 14 add D5W or D10W

  12. Cerebral edema • Rare, 7/1000 episodes, 30% mortality • Children under 5, new diagnosis DM with DKA • Present with improving DKA and then sudden deterioration • Pathophysiology unknown • No clear link to fluids, OR • Hypoxia • Volume depletion • Hyperosmolar state • Initial glucose • Ketones

  13. Cerebral Edema • Case Control study in kids NEJM: • Negative trend in sodium (kids with cerebral edema often have lower Na) • Clinical associations with CE • Lower initial pCO2 • every decrease 7.8mm = RR 3.4 (1.9-6.3) • Higher initial BUN • every increase 3.2 = RR 1.7 (1.2-2.5) • Therapeutic • Treated with HCO3 = RR 4.2 (1.5-12.1) Glaser N. 2001, NEJM

  14. Treatment • ABC • Elevate head of bead • Hyperventilate (patient probably already doing this) • Mannitol: 0.2-1 g/kg over 30 minutes • CT head • Decrease IV rate • ICU

  15. Best practice • Reduce osmolality slowly (< 3 mmol/ kg/ hr) • Don’t allow plasma Na to fall • No bicarb

  16. Potassium • Total body deficit of 3-5 meq/kg • Every treatment for DKA will decr K • K < 3.3 = NO INSULIN, give 40 meq/L, give po K. EKG • K 3.3-5.0 = 20-30 meq/L KCL with NS and may start insulin • K > 5.0 = EKG, start insulin, recheck in 1 hour

  17. Insulin • Treats the acidosis and ketosis • No benefit to bolus • Infusion Humulin R 0.1 mg/kg /hr • Goal = drop glucose 3-4 mmol / hour • Double insulin rate if goal not achieved • Cut insulin rate in half if decreasing too quickly

  18. Bicarbonate • Consider if • pH < 7 (after 1 hour of hydration) • hypotension, shock, coma • severe hyperkalemia with ECG changes • Complications from Bicarb: • Worsens CNS intracellular acidosis • shifts oxy-hemoglobin dissociation curve to left – worsens oxygen release in tissues • decreases serum K • may produce alkalosis / dysrhythmias • inhibits metabolism of ketones • ? cerebral edema

  19. A final word on bicarb • Patients treated with bicarb do no better, and possibly worse • Even in severe DKA pH 6.9-7.1 • It’s possible to manage DKA with fluids and insulin alone

  20. Hyperglycemic Hyperosmolar Non-ketotic State • Hyperglycemia, hyperosmolarity, dehydration and decreased mental status • Spectrum of disease with DKA • Relative insulin resistance with poor renal fxn • decreased renal clearance of glucose • Fluid shifts from ICF to ECF • Fluid lost in osmotic diuresis • Insufficient oral intake to compensate for losses

  21. HHNKS • Profound dehydration (8-12L) • Very high BG • BUN > 50 • Serum osmoles > 350 • No acidosis (bicarb > 15) • No ketosis

  22. Mr. M • 45 M in code room at PLC restrained by 4 security guards • Extremely agitated, diaphoretic, multiple contusions and laboured breathing • Family called EMS because he went beserk and threw a chair across the room

  23. Case • After handcuffs were removed, pt had a focal seizure beginning in R hand and progressed to generalized • Post-ictal: 120/80, 120, 24, 36.8 • Lethargic, oriented • R hemiparesis, R facial paralysis, R plantar extension • BG 1.8 at time of seizure

  24. 100cc D50W  5 minutes later patient’s neuro findings disappeared. • Hx: family physician placed him on a “diabetes” medication 2 weeks ago • Started on a drinking binge a few days ago.

  25. Catecholamine release Tremor Tachycardia Diaphoresis Piloerection Anxiety Hypertension HA Dry mouth Hunger Nausea Angina Neuroglycopenia Blurred vision Paresthesias Loss of coordination Poor concentration Somnolence Altered behaviour Hypothermia Seizures Hemiplegia Coma Death Manifestations of Hypoglycemia

  26. OHAs • Sulfonylureas (insulin secretagogue) • Glyburide (Diabeta), gliclazide (Diamicron) • Biguanides (inhibits gluconeogenesis) • Metformin • Glitazones (Decreases insulin resistance by increasing uptake into liver, adipose and skeletal muscle) • Rosiglitazone (avandia), pioglitazone (Actos) • Acarbose (Prandase) • Prevents degradation of complex carbs • Meglitinide (insulin segretagogue) • Repaglinide (Prandin)

  27. Sulfonylureas • Main culprit in OHA hypoglycemia • T ½ 18-24 hours • Requires 24 hours of monitoring • Often refractory to glucose administation – stimulates more insulin secretion

  28. Who gets hypoglycemia? • RF = overdose, elderly, renal disease, hepatic disease, multiple drugs • Precipitants in Diabetics: • Ethanol • Propanolol (B-adrenergic antagonist) • Salicyclates • Addison’s • Malnutrition

  29. Management of Mr. M • ABCs • Consider charcoal • FEED • IV D5*1/2NS at 150cc/hour to keep euglycemic • With boluses of 2cc/kg of D50W (ie. 1 amp) • Octreotide 50ug sc q6h

  30. Dextrose, etc • Po intake • 1 amp D50W (25g glucose) • Children: • D25W 0.5-1.0 g/kg • Neonates D10W • Glucagon 1-2 mg IM/sc if no IV access • 0.025-0.1 mg/kg children • Onset 10-20 min • Duration 30-60 min

  31. Octreotide • Synthetic somatostatin • t ½ 72 min • Inhibits B-cell insulin release stimulated by glucose • Fewer episodes recurrent hypoglycemia • Lower dextrose requirements overall • 50 ug sc/IV q6h • Few side effects

  32. Disposition • Who needs admission? • Intermediate and long-acting insulin • Persistent hypoglycemia with short acting • OHAs – sulfonyureas/meglitinide • Complicated Type 1 DM • Overdoses/social factors • Hepatic/renal failure

  33. OHAs and IV contrast • 55 yo F needs a CT Scan to diagnose possible appendicitis. • On Metformin and Avandia for DM • What do you do? • Risk of acute tubular necrosis • Check renal function • Hold Metformin 72 hours after until Cr checked again

  34. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Canadian Medical Assoication Journal April 2003, vol 168(7). • 2008 Clinical Practice Guidelines. Canadian Journal of Diabetes 2008: Sept, vol 32 (1 Suppl). • American Diabetes Association Clinical Practice Guidelines. Diabetes Care 2003; 26 (1 Suppl): S109-17 • Glaser N. et al. Risk factors for cerebrel edema in children with diabetic ketoacidosis. NEJM 2001. • Viallon A. et al. Does bicarbonate therapy improve the management of severe DKA? Crit care med 1999: 27( 2690). • Boyle PJ et al. Octreotide reverses hyperinsulinemia and prevents hypoglycemia induced by sulfonyurea overdoses. J Clin Endocrin Metab 1993; 76: 752-756.

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