DKA

1. DKA Carolyn Stickney July 10, 2008

2. DKA Defined Diabetic – glucose >250 mg/dL Keto – ketones produced Acidosis – anion gap metabolic acidosis; HCO3- <15, pH<7.30 most times glucose 500-800 in DKA ketones – both in urine and in serum (acetoacetate, acetone, betahydroxybutyrate – fruity smell, not often encountered in real life) consider that if these criteria aren’t met, it may not be DKAmost times glucose 500-800 in DKA ketones – both in urine and in serum (acetoacetate, acetone, betahydroxybutyrate – fruity smell, not often encountered in real life) consider that if these criteria aren’t met, it may not be DKA

3. Why does it happen? elevation of counter-regulatory hormones with concomitant reduction of insulin’s effective action hormones induce: hepatic/renal glucose production and impaired peripheral utilization ? hyperglycemia lipolysis and fatty acid oxidation ? ketone bodies name the counter-regulatory hormones: glucagon, cortisol, catecholamines, GH renal and hepatic gluconeogenesis (glucagon and increased availability of precursors like glycerol and alanine)name the counter-regulatory hormones: glucagon, cortisol, catecholamines, GH renal and hepatic gluconeogenesis (glucagon and increased availability of precursors like glycerol and alanine)

4. Yeah, but why does it happen? non-compliance/iatrogenic insulinopenia infection, infection, infection pneumonia, UTI, gastroenteritis thromboembolic phenomena: MI, CVA, etc. new-onset disease pancreatitis trauma or alcohol abuse common mistakes: omitting insulin in the setting of gastro/acute illness inability to keep up with hydration MI is a very common cause – think, DM pts are at higher risk of CV disease at baseline cocaine abuse! new-onset disease CAN occur at any age, though there are clearly peakscommon mistakes: omitting insulin in the setting of gastro/acute illness inability to keep up with hydration MI is a very common cause – think, DM pts are at higher risk of CV disease at baseline cocaine abuse! new-onset disease CAN occur at any age, though there are clearly peaks

5. “DKA” isn’t going to be their chief complaint, right? nausea/vomiting abdominal pain lethargy or fatigue polyuria/polydipsia and subjective dehydration symptoms of precipitating event DKA usually evolves rapidly over 24 hours or less abdominal pain is multifactorial – dehydration of muscle tissue, delayed gastric emptying, ileus from electrolyte disturbances, metabolic acidosis; very common in children, but still seen in adults, sometimes even mimicking acute abdomen if does not resolve with resolution of DKA, need to investigate furtherDKA usually evolves rapidly over 24 hours or less abdominal pain is multifactorial – dehydration of muscle tissue, delayed gastric emptying, ileus from electrolyte disturbances, metabolic acidosis; very common in children, but still seen in adults, sometimes even mimicking acute abdomen if does not resolve with resolution of DKA, need to investigate further

6. Lab Evaluation(or, what the ER should have sent) glucose generally <800, but will often be “crit hi” in ED abnormalities to expect: leukocytosis even >20K, with left shift (but usually <10% bands), hyponatremia (pseudo vs real), K abnl, elevated BUN/Cr, AGMA; glucose, ketones on u/a; primary metabolic acidosis with resp comp don’t forget the all-important gap: how big is it? what’s a normal gap? how do you measure it?glucose generally <800, but will often be “crit hi” in ED abnormalities to expect: leukocytosis even >20K, with left shift (but usually <10% bands), hyponatremia (pseudo vs real), K abnl, elevated BUN/Cr, AGMA; glucose, ketones on u/a; primary metabolic acidosis with resp comp don’t forget the all-important gap: how big is it? what’s a normal gap? how do you measure it?

7. Your chance to think cultures: urine, blood, sputum, etc. chest X-ray cardiac enzymes, EKG LFTs, amylase/lipase ß-HCG other imaging given clinical suspicions other common infectious etiologies to think about: wound infection (decub? foot/leg ulcers?), PID (ew) remember that silent ischemia is more common in diabeticsother common infectious etiologies to think about: wound infection (decub? foot/leg ulcers?), PID (ew) remember that silent ischemia is more common in diabetics

8. While you’re waiting… FLUIDS! total deficit on presentation commonly 5-10 L start with NS resuscitation even after restoration of adequate circulation, high rates of IVF infusion further osmotic diuresis will occur will help decrease serum glucose signs you are really behind to begin with: hypotension, oliguria… shock can usually switch to 1/2NS after initial resuscitation – but if hyponatremic, would use NS increasing renal perfusion helps osmotic diuresis, also hemodilution effectsigns you are really behind to begin with: hypotension, oliguria… shock can usually switch to 1/2NS after initial resuscitation – but if hyponatremic, would use NS increasing renal perfusion helps osmotic diuresis, also hemodilution effect

9. Diabetics need insulin initial bolus of IV insulin: 0.1-0.15 units/kg continuous infusion 0.1 units/kg/hr goal: decrease blood sugar ~50-75 mg/dL/hr titrate insulin based on finger sticks, but… goal decrease – means you have to check glucose hourly, at least initiallygoal decrease – means you have to check glucose hourly, at least initially

10. When the glucose falls once chem sticks fall below 200-250 mg/dL, add dextrose to fluids fixing the sugar isn’t the endgame need to keep glucose ~200 mg/dL until you’ve closed the gap: Na+ - (Cl- + HCO3-) <12 this means monitoring chemistries frequently (renal panel a good choice) like fluids aren’t just for dehydration, insulin isn’t just for sugar – it cuts down on lipolysis and may improve ketone utilization when you get to this range of d-sticks, you may need to decrease your drip as well, particularly if you had to titrate it higher initially frequent renal panels will also allow you to keep an eye on your other electrolytes you can also look at urine dips for ketoneslike fluids aren’t just for dehydration, insulin isn’t just for sugar – it cuts down on lipolysis and may improve ketone utilization when you get to this range of d-sticks, you may need to decrease your drip as well, particularly if you had to titrate it higher initially frequent renal panels will also allow you to keep an eye on your other electrolytes you can also look at urine dips for ketones

11. Osmotic diuresis = electrolyte depletion urine losses are free water >> sodium serum sodium usually low to normal – beware of pseudohyponatremia remember correction factor (1.6 mEq/100 mg/dL glucose above 100) potassium – “hyperkalemia” can be deceiving once adequate urine output ensured, add KCl to IVF (20-40 mEq/L) potassium: urinary losses, but looks high because of insulin deficiency, hyperosmolality, acidosis forces potassium extracellularly if already hypokalemic on presentation, need to aggressively replete K, particularly since you want to give insulin, which is only going to drive serum K lower if hypomag on presentation, treat this as well (hard to maintain normokalemia in face of hypomagnesemia)potassium: urinary losses, but looks high because of insulin deficiency, hyperosmolality, acidosis forces potassium extracellularly if already hypokalemic on presentation, need to aggressively replete K, particularly since you want to give insulin, which is only going to drive serum K lower if hypomag on presentation, treat this as well (hard to maintain normokalemia in face of hypomagnesemia)

12. Electrolytes under debate hypophosphatemia is common as well no evidence that routine supplementation indicated in adults follow levels on renal panels bicarbonate drips don’t seem to affect outcome with pH 6.9-7.1 that said, drips are often used when pH<6.9 given risk of vascular compromise phos, like K, can be elevated on admission, but TB deficit is inevitable should supplement with P<1 (Kphos works in IVF) with acidosis that severe, your patient is going to be in the MICU, and you won’t have to make the decisionphos, like K, can be elevated on admission, but TB deficit is inevitable should supplement with P<1 (Kphos works in IVF) with acidosis that severe, your patient is going to be in the MICU, and you won’t have to make the decision

13. When the gap closes… think: can they eat yet? if no, continue insulin and dextrose infusions if yes, restart home regimen: give subcutaneous, turn off drip about an hour later don’t forget to order a diet! if new diagnosis, design an initial regimen and titrate as necessary (total insulin requirements ~0.5-0.8 units/kg/day) remember: just because the crisis is over, it doesn’t mean that the pt doesn’t need glucose (and thus insulin) if they can’t eat, why not? don’t overlook that – abdominal pain/N/V due only to DKA should resolve with crisis if you’re not at their regularly scheduled insulin dosing time, you’re going to have to make it up a little until the time of the next regularly-scheduled dose if in doubt about patient’s ability to eat, play it safe and decrease subq dose, but don’t eliminate altogether also, don’t forget to keep monitoring glucose more frequently than ac/hs for the first six to eight hours… in new diagnoses… beware the ketosis-prone type II diabeticremember: just because the crisis is over, it doesn’t mean that the pt doesn’t need glucose (and thus insulin) if they can’t eat, why not? don’t overlook that – abdominal pain/N/V due only to DKA should resolve with crisis if you’re not at their regularly scheduled insulin dosing time, you’re going to have to make it up a little until the time of the next regularly-scheduled dose if in doubt about patient’s ability to eat, play it safe and decrease subq dose, but don’t eliminate altogether also, don’t forget to keep monitoring glucose more frequently than ac/hs for the first six to eight hours… in new diagnoses… beware the ketosis-prone type II diabetic

14. What can go wrong majority of morbidity and mortality is from precipitating events hypoglycemia hyperglycemia hypokalemia, hypophosphatemia noncardiogenic pulmonary edema cerebral edema (young patients) e.g. infection, MI, CVA, etc. overdoing the insulin drip bad subcutaneous transition – i.e. not giving pulm edema thought to occur because of decrease colloid oncotic pressure, more water leak in lungs, decreased compliance cerebral edema is multifactorial and not JUST because of over-rapid correction of extracellular sodium must, must monitor mental status in these patients – almost all cases are in patient less than 20 years olde.g. infection, MI, CVA, etc. overdoing the insulin drip bad subcutaneous transition – i.e. not giving pulm edema thought to occur because of decrease colloid oncotic pressure, more water leak in lungs, decreased compliance cerebral edema is multifactorial and not JUST because of over-rapid correction of extracellular sodium must, must monitor mental status in these patients – almost all cases are in patient less than 20 years old

15. Bottom line necessities fluids – be aggressive insulin – monitor hourly glucose levels, watch for closure of AG electrolytes – frequent renal panels precipitating event – treat the infection or MI