Today we discussed DKA. This potentially life-threatening problem is a relatively common internal medicine referral, and although most cases are straightforward, there are a few points to keep in mind to ensure optimal management.
Pathophysiology:
Requires insulin deficiency and increased counterregulatory hormones. Often triggered by inadequate insulin dosing, surgery, infarction (e.g. MI, mesenteric, etc.), infection, steroids. Always search for the precipitant of DKA!
Points on history:
1) History of hyperglycemia: polydypsia, polyuria, polyphagia, visual blurring
2) History suggestive of DKA itself: abdominal pain is common, tachypnea, nausea
3) History of volume depletion: Presyncope, postural symptoms
4) Search for precipitant: Chest pain, abdominal pain, medications, intoxications, insulin use (ar lack thereof...)
Points on physical:
Physical examination may or may not demonstrate depressed sensorium. Typical findings include tachypnea with Kussmaul’s respiration, tachycardia, frank hypotension or orthostatic blood pressure changes, the odor of acetone on the breath, and signs of volume depletion.
Labs:
Ordered on most patients would be
Glucose, cbc+diff, lytes, ABGs, serum ketones, urine dipstick, Cr, BUN, tox screen, lactate, troponin, ECG, CXR
Monitors: 2 large bore IVs, ECG, foley, possibly art line.
3 Common errors in DKA management:
1) Mismanagement of K+ is the main reason for mortality in these patients. The K+ may be normal because of shifting out of cells from acidosis and lack of insulin, but patients are total body depleted because of urinary losses from polyuria and increased aldosterone. Starting with normal K+ is concerning, and starting with low K+ is very concerning, and that patient may need ICU for central line to deliver K+
2) The main problem in DKA is not hyperglycemia, it is ketoacidosis. The insulin drip is to treat the anion gap (i.e. the ketoacidosis), not the hyperglycemia. If the patient has a high anion gap and normal glucose, continue the insulin and add glucose.
3) Transition to SC insulin after infusion is an issue. Remember that the halflife of IV insulin is minutes, and you therefore need to overlap SC with IV, usually for several hours (until the effect of the SC insulin) before turning infusion off. Transition to SC when anion gap is normal, glucose is controlled, IV insulin dose is stable, and patient is eating. Remember that SC insulin is half as bioavailable as IV.
Management:
Major issues (not necessarily in this order; depends on specific situation) are:
Pathophysiology:
Requires insulin deficiency and increased counterregulatory hormones. Often triggered by inadequate insulin dosing, surgery, infarction (e.g. MI, mesenteric, etc.), infection, steroids. Always search for the precipitant of DKA!
Points on history:
1) History of hyperglycemia: polydypsia, polyuria, polyphagia, visual blurring
2) History suggestive of DKA itself: abdominal pain is common, tachypnea, nausea
3) History of volume depletion: Presyncope, postural symptoms
4) Search for precipitant: Chest pain, abdominal pain, medications, intoxications, insulin use (ar lack thereof...)
Points on physical:
Physical examination may or may not demonstrate depressed sensorium. Typical findings include tachypnea with Kussmaul’s respiration, tachycardia, frank hypotension or orthostatic blood pressure changes, the odor of acetone on the breath, and signs of volume depletion.
Labs:
Ordered on most patients would be
Glucose, cbc+diff, lytes, ABGs, serum ketones, urine dipstick, Cr, BUN, tox screen, lactate, troponin, ECG, CXR
Monitors: 2 large bore IVs, ECG, foley, possibly art line.
3 Common errors in DKA management:
1) Mismanagement of K+ is the main reason for mortality in these patients. The K+ may be normal because of shifting out of cells from acidosis and lack of insulin, but patients are total body depleted because of urinary losses from polyuria and increased aldosterone. Starting with normal K+ is concerning, and starting with low K+ is very concerning, and that patient may need ICU for central line to deliver K+
2) The main problem in DKA is not hyperglycemia, it is ketoacidosis. The insulin drip is to treat the anion gap (i.e. the ketoacidosis), not the hyperglycemia. If the patient has a high anion gap and normal glucose, continue the insulin and add glucose.
3) Transition to SC insulin after infusion is an issue. Remember that the halflife of IV insulin is minutes, and you therefore need to overlap SC with IV, usually for several hours (until the effect of the SC insulin) before turning infusion off. Transition to SC when anion gap is normal, glucose is controlled, IV insulin dose is stable, and patient is eating. Remember that SC insulin is half as bioavailable as IV.
Management:
Major issues (not necessarily in this order; depends on specific situation) are:
1) volume 2) electrolytes (esp. K+) 3) insulin 4) acid/base status
1. IV fluids: Start with 1L NS wide open. Make sure urine output. General teaching is 1L in 30 min then 1L in 1h. When glucose reaches 12-14, change to D5W with 1/2 NS and decrease insulin to 0.05U/kg/h. Maintain glucose at this level until DKA is resolved and pt is alert. Avoid giving hypotonic solutions because of risk of brain edema (seen more in kids) which comes from shifts in glucose without accmpanying change in Na.
2. K, PO4: If K less than 3.3mM, hold insulin, give 40mM K per liter of IV fluid until K is greater than 3.3. If K is above 5.5, do not give K, but check level q2h. If K is between 3.3 and 5, give 20-40mM K in IV fluid to keep K at 4-5mM, possibly with additional K po. Give K before insulin anticipating fall if it is low to begin with. Remember that phosphate also gets shifted (like K) and if gets very low may cause rhabdo, severe muscle weakness, CHF, etc. Replace it.
3. Insulin (IV): Bolus 0.1u/kg, then 0.1U/kg/h. Check glucose hourly. If it does not fall by 3mM in 1st hour, double insulin dose hourly until steady drop of 3-4mM/h. See above for when glucose=12-14. After resolution, check glucose q4h and start SC insulin. Insulin continues until AG normalizes.
4. Acid/base: In general bicarb not required unless pH is less than 7.0. If so, may give amps or dilute 3 amps NaHCO3 in 850mL D5W, and infuse 150-200mL/h.
Control N/V with IV Gravol
Many people find it convenient to manage DKA by a flowchart updated ~hourly (although not everything needs to be checked hourly). You may want to record:
Time, Vitals, urine output, pH, HCO3, AG, Ket, Glu, K, PO4, IV fluid rate, insulin dose
A couple of extra points:
-Na for anion gap calculation is not adjusted for glucose.
-Expect to see non-anion gap metabolic acidosis after AGMA resolves, because of loss of ketone bodies without H+ (i.e. loss of anion alone)
Link:
Click here for a CMAJ review article on DKA that also compares and contrasts with diagnosis and management of HONK
1. IV fluids: Start with 1L NS wide open. Make sure urine output. General teaching is 1L in 30 min then 1L in 1h. When glucose reaches 12-14, change to D5W with 1/2 NS and decrease insulin to 0.05U/kg/h. Maintain glucose at this level until DKA is resolved and pt is alert. Avoid giving hypotonic solutions because of risk of brain edema (seen more in kids) which comes from shifts in glucose without accmpanying change in Na.
2. K, PO4: If K less than 3.3mM, hold insulin, give 40mM K per liter of IV fluid until K is greater than 3.3. If K is above 5.5, do not give K, but check level q2h. If K is between 3.3 and 5, give 20-40mM K in IV fluid to keep K at 4-5mM, possibly with additional K po. Give K before insulin anticipating fall if it is low to begin with. Remember that phosphate also gets shifted (like K) and if gets very low may cause rhabdo, severe muscle weakness, CHF, etc. Replace it.
3. Insulin (IV): Bolus 0.1u/kg, then 0.1U/kg/h. Check glucose hourly. If it does not fall by 3mM in 1st hour, double insulin dose hourly until steady drop of 3-4mM/h. See above for when glucose=12-14. After resolution, check glucose q4h and start SC insulin. Insulin continues until AG normalizes.
4. Acid/base: In general bicarb not required unless pH is less than 7.0. If so, may give amps or dilute 3 amps NaHCO3 in 850mL D5W, and infuse 150-200mL/h.
Control N/V with IV Gravol
Many people find it convenient to manage DKA by a flowchart updated ~hourly (although not everything needs to be checked hourly). You may want to record:
Time, Vitals, urine output, pH, HCO3, AG, Ket, Glu, K, PO4, IV fluid rate, insulin dose
A couple of extra points:
-Na for anion gap calculation is not adjusted for glucose.
-Expect to see non-anion gap metabolic acidosis after AGMA resolves, because of loss of ketone bodies without H+ (i.e. loss of anion alone)
Link:
1 comment :
Team it is very useful article, Keep it up
Diabetes Ketoacidosis Treatment
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