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DKA

DKA. Crystal Lantz PGY3. Pathogenesis 1. Lack of insulin production prevents glucose uptake by muscle and allows unrestrained hepatic glucose production.

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DKA

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  1. DKA Crystal Lantz PGY3

  2. Pathogenesis 1 • Lack of insulin production prevents glucose uptake by muscle and allows unrestrained hepatic glucose production. • Lack of suppression of lipolysis leads to excess circulating FFAs which are converted into ketoacids (B-OH-butyrate and acetoacetate) by the liver.

  3. Pathogenesis 2 • This leads to acidemia which may impair vascular tone and cardiac function. • Marked hyperglycemia and ketonemia cause osmotic diuresis with loss of water and electrolytes.

  4. History 1 • Nausea, emesis • Abdominal pain (2/2 delayed gastric emptying/ileus 2/2 acidosis and lyte abnormalities and may correlate with degree of acidosis) • Polyuria/Polydipsia • Lethargy • Headache • Anorexia • Usually develop over 24h or less in DKA; over multiple days more insidiously in HHS.

  5. History 2 • Possible precipitating events (“Is”) • Infection (UTI? PNA?) • Insulin (incorrect dosing/noncompliance) • Ischemia (myocardial….mesenteric) • Initial presentation of DM.

  6. History 3 • More uncommon causes • Med effect – meds that affect carb metabolism • Steroids • High-dose thiazides • Atypical antipsychotics • CVA • Pancreatitis • Cocaine use

  7. DKA can develop after admission for something else… • In hospitalized pts without DKA who present with CVA, MI, or infection and glucose >250… • Maintain high suspicion for DKA – check RFP for AG and serum/urine ketones.

  8. Physical 1 • ABCs • Mental status • Evidence of intercurrent illness (infection, MI, CVA, pancreatitis) • Abdominal exam – TTP, hypoactive BS • Volume status • Skin turgor • Mucosa • Flat neck veins • Orthostatic hypotension

  9. Labs/Imaging… • RFP – for lytes, glc, CALCULATE AG • CBC • UA/ketones • Plasma osmolality • Serum ketones if urine ketones are present (B-OH-Butyrate, Acetone, Acetaoacetate) • ABG if serum HCO3 reduced • ECG • Consider infectious w/u(blood, urine, sputum, CXR) • HbA1C may be useful

  10. Diagnosis

  11. B-OH-Butyrate  Acetone & Acetoacetate • Direct measurement of B-OH-Butyrate is preferable for monitoring degree of ketonemia and is available at UHCMC (not VA) • Standard ketones may become increasingly positive as conversion from B-OH-Butyrate to acetone/acetoacetate occurs

  12. Switching gears to an Acid-Base talk… • 5 Step Approach to ABGs without memorizing formulas….

  13. Identify alkalosis/acidosis by pH change from 7.4. (>7.4 = alkalosis. <7.4 = acidosis). • Determine if primary disorder is respiratory or metabolic based on direction of change of PCO2. If pH and PCO2 change in same direction - metabolic If pH and PCO2 change in opposite direction - respiratory

  14. 3. Check compensation to identify other primary disorders. Metabolic Acidosis - Check Resp Compensation. PCO2 = (1.5 × [HCO3-]) + 8 ± 2 Simplified: For every 1 mEq decrease in HCO3, PCO2 should decrease by 1.2 mmHg. Example: If HCO3 is 9...24-9 = 15. PCO2 reduction should be 15x1.2 = 18. 40-18 = 22mmHg. Metabolic Alkalosis – Check Resp Compensation. PCO2 rises 0.7mmHg for each 1.0 mEq rise in HCO3. Example: If HCO3 is 34...34-24 = 10. 10 x 0.7 = 7. 40+7 = 47mmHg.

  15. Acute Respiratory Acidosis: Every 10 mmHg rise in PCO2 = 1 meq rise in HCO3 Chronic Respiratory Acidosis: For every 10 mmHg rise in PCO2 = 3.5 mEq rise in HCO3

  16. Acute Respiratory Alkalosis: Every 10 mmHg drop in PCO2 = 2 meq drop in HCO3 Chronic Respiratory Alkalosis: For every 10 mmHg drop in PCO2 = 5 mEq drop in HCO3

  17. 4. If metabolic acidosis - calculate anion gap. Na - (Cl+HCO3) Normal gap 12 or less. For each gram of albumin drop less than 4 add 2.5 to calculated gap to get actual gap. Example: Calculated gap 9. Albumin 2. Add 5 to gap = 14.

  18. 5. If AGMA - calculate delta gap. Change in gap divided by change in bicarbonate. (AG-12) / (24-HCO3) <1 – AGMA + NAGMA 1-2 - Pure AGMA >2 – AGMA + Metabolic Alkalosis

  19. In DKA, initially AGMA; as treatment proceeds many will develop a subsequent NAGMA. • Ketoacid anions are excreted in the urine with sodium which would have been used to reproduce HCO3 in the kidney  loss of “potential HCO3” which is equivalent to actual bicarb loss  subsequent NAGMA.

  20. Serial Monitoring • Q1H POCT Glucose until stable • RFP/Serum osmolality q2-4h with close FU of HCO3. • Consider VBG rather than frequent ABGs for pt and intern comfort – venous pH is about 0.03 units lower than ABG.

  21. DKATx

  22. HHS Tx

  23. Fluids, fluids, fluids. • Severe Hypovolemia – NS 1000cc/h • Milder Dehydration – evaluate corrected Na (Corrected Na = Measured Na (Glc-100/100) • Hyponatremia – 250-500cc/h NS • Normal-Hypernatremia – 250-500c/h 1/2NS When serum glc reaches 200 (or 300 in HHS)  Change to D51/2NS 150-250cc/h

  24. Insulin therapy 1 • Usually IV route except in mild DKA. • IV: Regular insulin 0.1U/kg bolus then 0.1U/kg/h continuous infusion OR no bolus with infusion rate alone at 0.14U/kg/h • SQ: Lispro 0.3U/kg x1 then 0.2U/kg in 1hr then 0.2U/kg SQ q2h. • If serum glc doesn’t fall by 50-70 mg/dL in 1st hour double the IV or SQ dose. • K <3.3 is a CONTRAINDICATION to insulin.

  25. Insulin therapy 2 • When glc to 200 (in DKA) or 250-300 (in HHS) reduce infusion to 0.02-0.05U/kg/h IV or change SQ dosing to 0.1U/kg q2h with goal glc 150-200. • Never discontinue insulin prior to closure of anion gap!

  26. Potassium therapy… • If K <3.3 – hold insulin therapy and replete K with fluids – 40-60mEq/h to ½NS until K 3.3+ (assuming UOP 50cc/h+). • If K >5.3 – no K supplementation but check q2h. • 3.3-5.3 – Give 20-30mEq per liter of 1/2NS goal K 4-5 (assuming UOP 50cc/h+). • Substantial losses in almost all 2/2 urine loss; shifts out of cells 2/2 insulin deficiency and hyperosmolality so K artifically elevated at presentation.

  27. Phosphate? • Whole body PO4 depletion is common though PO4 will be normal or elevated initially due to migration out of cells. • With treatment hypophosphatemia will develop usually without adverse effects in a self-ltd fashion. • No benefit to repleting PO4 unless cardiac dysfx/hemolytic anemia/resp depression, concentration <1.

  28. Assess need for HCO3… • pH <6.9  Consider HCO3 gtt (though small studies have shown minimal benefit…) • pH >7.0  No HCO3

  29. Resolution… • Ketoacidosis resolved – AG is normal (<12) • Ketonemia/Ketonuria may persist >36h without pt actually being in true ketoacidosis. • HHS pts are mentally alert and plasma osmolality is <315. • Pt is able to tolerate PO.

  30. What to do with the insulin gtt when gap has closed… • Initiate SQ insulin AT MEALTIME with a 1-2h taper of the gtt. • Insulin Naïve  0.5-0.8U/kg per day in sliding scale + long-acting regimen • 25% as long acting. • 25% as scheduled meal-time insulin • Sliding Scale • Known DM  start at previous insulin regimen.

  31. Potential Complications 1 • Cerebral edema • Very rare in adults but 40% mortality. • Sxs: ha, lethargy, decreased arousal  seizures, incontinence, brady, resp arrest, pupul changes. • Mortality 20-40%. • Prevented by following protocol, adding dextrose to fluids when appropriate. • Tx – unit, mannitol?, 3%NS?

  32. Potential Complications 2 • Non-cardiogenic pulmonary edema • Hypoxemia 2/2 decreased osmotic pressure  migration of fluid into lungs. • If initial A-a gradient is widened on ABG, higher risk of development of pulmonary edema.

  33. A 23-year-old woman with type 1 diabetes mellitus is admitted to the hospital with a diagnosis of community-acquired pneumonia and lethargy. Before admission, her insulin pump therapy was discontinued because of confused mentation. On physical examination, temperature is 37.5 °C (99.5 °F), blood pressure is 108/70 mm Hg, pulse rate is 100/min, and respiration rate is 24 min. There are decreased breath sounds in the posterior right lower lung. Neurologic examination reveals altered consciousness.

  34. Sodium 130 meq/L (130 mmol/L) • Potassium 5.0 meq/L (5.0 mmol/L) • Chloride 100 meq/L (100 mmol/L) • Bicarbonate 16 meq/L (16 mmol/L) • Blood urea nitrogen 38 mg/dL (13.6 mmol/L) • Creatinine 1.4 mg/dL (123.8 µmol/L • Glucose 262 mg/dL (14.5 mmol/L) • Urine ketones Positive

  35. Which of the following is the most appropriate next step in management? A Add insulin glargine B Add neutral protamine Hagedorn (NPH) insulin C Implement a sliding scale for regular insulin D Start an insulin drip

  36. Questions?

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