Diabetic Ketoacidosis (DKA)

Learning Objectives
1.Diagnosis of DKA
2.Precipitants of DKA
3.Managment of DKA
4. LADA- late onset autoimm. diabetes of adulthood

DKA is most common in DM1 but can occur in DM2 when under significant stress.
Normally, insulin allows tissue (mostly muscle) to take up glucose and suppresses lipolysis and proteolysis (anabolic state)
When under stress and with insulin deficiency, the body produces glucagon-> glycogenolysis-> hi blood glucose
and increases lipolysis-> FFA like beta hydroxybutyrate and acetoactone which cause acidosis(catabolic state)

Lab abnormalities:
hi bg (blood glucose), agap acidosis, ketonemia, ketonuria
"serum ketone" tests measure acetoacetone, which is just one of the 2 major ketones
serum b- hydroxybutyrate is a more accurate test of ketonemia but less readily available
ketonuria can have false positive with some drugs ie) captopril
K+ may be high in serum due to acidemia causing extracellular shifts, but pt have overall low K+
BUN and creatinine may reflect dehydration as glucosuria causes osmotic diuresis
PE: fruity breath (acetone), kussmaul's respirations (deep labored), tachycardia, hypotension

Triggers:
Infection ie) influenza, pneumonia, gastroenterits
Significant stressors: ACS, CVA, drugs (cocaine, meth)
Noncompliance: insulin pump dysfunction, insulin noncompliance
Will Daines gave us a nice tool: "6 i's"causing dka
infection, ischemia, insulin deficiency, intra-abd processes (compromising pancreatic function), iatrogenic (ie) steroids), and ingestions (meth, cocaine)

Management of DKA
1.Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis).

2.Admit to hospital; ICU may be necessary for frequent monitoring or if pH < 7.00 or AMS

3.Assess:
Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate)
Acid-base status—pH, HCO3-, PCO 2 , b-hydroxybutyrate
Renal function (creatinine, urine output)

4.Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour); subsequently, 0.45% saline at 150–300 mL/h; change to 5% glucose and 0.45% saline at 100–200 mL/h when plasma glucose reaches 250 mg/dL (14 mmol/L).

5.Administer short-acting insulin: IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h. If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do not administer insulin until the potassium is corrected to > 3.3 mmol/L (3.3.meq/L).

6.Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).

7.Measure capillary glucose every 1–2 h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.

8.Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1–4 h.

9.Replace K+: 10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flow and normal creatinine documented; administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if bicarbonate is given.

10.Continue above until patient is stable, glucose goal is 150–250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.

11.Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection.

(Ellen Eaton MD, 9/30/10)