DIABETIC KETOACIDOSIS

Page by: E.J. Mayeaux, Jr., M.D.
Louisiana State University Medical Center Shreveport, Louisiana

Presentation 1. DKA often presents as anorexia, N/V, and abdominal pain. a. Abdominal pain be sufficiently severe to suggest an acute surgical abdomen. b. Abdominal tenderness, guarding, decreased bowel sounds, and increased WBC may be present. c. Abdominal pain 2o DKA almost always subsides in 6-8 hours after institution of therapy. 2. DKA is often preceeded by a period of polvdipsia, polyphagia, polyuria, weight loss, increasing weakness, and mental obtundation. 3. The onset is usually gradual over several days. 4. Hypothermia is the rule and does not preclude infection. DIFFERENTIAL DIAGNOSIS DKA HYPOGLYCEMIA Onset Gradual Sudden Skin Warm, dry Cool, clammy Respirations Rapid and deep Not deep, but (Kussmal) may be rapid not as profound Very profound Breath Odor Sweet, fruity DKA MNKC Ketosis Present Absent Blood sugar Usually < 600 Usually > 900 Never < 600 Osmolarity Usually < 350 Usually > 350 ~ 28 ~ 80 Na+ Usually low Usually high Metabolic acidosis Usually severe Usually not severe ( acidosis < 7.35 ) PRECIPITATING FACTORS (There is always a precipitating factor) 1. Infection - most common - usually UTI, URI, infected decubitus 2. Silent MI 3. Non-compliance is taking meds 4. Intraabdominal catastrophes 5. Pancreatitis (Note increased amylase seen in 2/3 of patients with DKA) 6. Stroke 7. Trauma, surgery, psychological stress MANAGEMENT ALWAYS MAKE A FLOW SHEET! Initial labs: 1. SMA-7 a. Glucose - use dextrostik initially and PRN. b. Bun - often increase 2o dehydration. c. Creatinine - may be increased out of proportion to BUN 2o interference by acetoacetate with picric acid in assay. 2. Acetone - Bedside: Dilute plasma 1:1 with NS or water and test with crushed acetest tablet; > 2+ reaction = significant ketosis (may use undiluted serum instead). 3. CBC a. HCT - often increase 2o dehydration. b. WBC - leukocytosis is common even without infections and may be masked. 4. ABG's 5. Calcium and Phosphorus - baseline 6. Lactate - Not increased in ordinary DKA; acidosis not accounted for by ketoacidosis may be 2o lactic acidosis, especially in elderly, hypotensive patients. 7. U/A - glucose, ketones, UTI Calculate: 1. Correct the Na+ for glucose For every 100 mg/dl increase in glucose > 100, add 2.5 mEq/l to the measured serum Na+. 2. Fluid deficit a. Normal TBW - 0.6 x IBW (kg) b. Current TBW - Normal serum Na+ (Normal IBW) Corrected serum Na+ c. Body water deficit - Nl TBW - Current TBW d. Correct half the deficit in the first 8 hours and the rest over the next 16-24 hours. 3. Serum Osmolarity 2 (corrected Na+) + (glucose) + (BUN) 18 2.8 - A patient in coma with osmolarity < 340 is probably not in DKA; look for stroke or severely decreased phosphate. Treatment: 1. FLUIDS - use NS or 1/2NS a. Use 1/2NS if: Corrected serum Na+ > 150 Bicarb is being given. Otherwise use NS initially. b. Usually give 1-2 liters over the first hour. c. Severe hypotension: may need albumin, whole blood, or continuous NS. d. Monitor CVP if: heart disease, renal disease, hypotension, elderly, susceptible to overload. e. Swan-Ganz catheter preferred if: severe shock, pulmonary hypertension, MI. f. Follow initial rapid hydration with 1/2NS at 300-500 cc/hr. 2. Insulin: a. Peak action of regular insulin: IV - 5-10 mins. IM - 1-2 hours SQ - 4 hours b. Two routes preferred: continuous IV or IM. c. Dose: 0.1 unit/kg/hr IV 0.1 unit/kg/dose IM 7 units/hour d. Give IV bolus of 10 - 20 units (0.33 units/kg) first (both routes) e. Continuous IV: 50 units in 250 cc 1/2NS - 1 unit/5cc via infusion pump at 35 cc/hour - (addition of albumin to set-up is not necessary) f. Measure glucose, acetone, electrolytes and ABG's every hour. g. Blood sugar should decrease 10% per hour or 100 mg/dl per hr. - if not, increase (double) the infusion rate or repeat the loading dose. h. At blood sugar = 250: switch to 5 units of insulin 250 cc D51/2NS, and continue the infusion until the plasma is cleared of ketones. - (Average dose is 50 units over 5 hours to decrease blood sugar to 250). i. Maintain the blood sugar at 250 and continue the infusion until the acidosis is corrected (pH normal). j. Criteria for stopping insulin infusion: (1) Normal pH (acidosis corrected) (2) Negative serum and urine acetone (3) Eating (4) Looks good and feels good k. The patient should be out of DKA in 10 - 16 hours. If not out of DKA in 16 hours there is an increased icidence of mucormycosis (headache, drainage of pink nasal secretions) l. To establish the insulin regimen: (1) Usually the patient will be clear by the next morning (2) If the infusion is still running give half of the previous insulin dose as NPH or give 0.1 units/kg of NPH as the a.m. dose (3) If the infusion is discontinued: (a) Begin sliding scale regular insulin SQ every 4 hours. OR: (b) Give 10 units NPH empirically as the AM dose. (most people will tolerate this dose). (c) Get 7 AM and 4 PM blood sugars daily. Regulate the insulin dose if the 4 PM blood Sugar is > 200. (d) When 4 PM blood sugar is < 200, get qid blood sugars (7 AM, 11 AM, 4 PM, and 10 PM) to refine dosage. 3. BICARBONATE a. Indications: (1) pH < 7.1 (2) Hypotension, shock or both when pH < 7.2 (3) Consider bicarbonate when low pCO2 (already maximally compensated) or lung disease (can't compensate) b. Dose: 2 amps (88 meq) diluted in 1 liter of l/2NS given over 1 - 2 hours. Repeat dose until pH > 7.2 c. Do not give as bolus unless unless in resuscitation, shock or if initial pH <7.0. 4. POTASSIUM a. Monitor q 1 hour. b. Make sure there is urine output. c. If K is normal or low, start K at once; if increased, give when K+ reaches 5.5 d. Give 40 mEq in the first liter and 20 - 40 mEq/L thereafter. 5. PHOSPHATE a. If possible, get an initial phosphate (and calcium) as a baseline and monitor every 4 - 6 hours. b. Decrease in phosphate will usually not be seen until 8 - 12 hours; replace phosphate if and when it falls to low levels. c. Prevention of hypophosphatemia in DKA (1) 20 mEq/L of K+ replacement may be given as K Phosphate. (2) K Phosphate = 4.4 mEq K+ + 3mmole phosphate/ cc (3) 5 cc of K phosphate/L = 22 mEq K+ + 15mmole (466 mg P) phosphate/L (4) Rate of K phosphate solution must not exceed 10mmole/hr. (5) Some authorities should give the first 10 - 30 mEq of K+ replacement as K phosphate. d. Danger of phosphate therapy is that too much phosphate binds calcium leading to hypocalcemia. e. Low phosphate leads to deficiency of ATP and 2.3 DPG which shifts the Hb dissociation to the left and impairs oxygen delivery to the tissues. 6. ADDITION MEASURES a. If obtunded: Endotracheal intubation prior to NGT to prevent aspiration b. Foley catheter if obtunded, urinary outlet obstruction, or oliguria after several hours of treatment. c. Tagamet 300 mg. IVPB every 8 hours to prevent stress ulcerations. d. Search for precipitating factors (1) Cultures (2) Spinal Tap (3) Serial EKG's and cardiac enzymes e. Cerebral Edema is a risk if fluid deficit is corrected too fast or if markedly hypotonic fluids are used. -Usually seen in adolescent diabetics. -S/S: progressive obtundation, increased ICP (papilledema, blown pupil), and hypothalamic dysfunction (hyperpyrexia, diabetes insipidus) f. Diet (1) Liquids when PO fluids tolerated (2) Regular ADA diet in 24 - 48 hours g. Monitor Calcium and Phosphate daily h. Unexplained or retractory shock: think of MI, sepsis, bowel infarction, or lactic acidosis. i. Remember that patients with lousy kidneys do not spill glucose! j. Sliding scale for glucometer: Blood sugar: > 400 Regular insulin SQ: 20 units > 300 15 units > 200 10 units

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