Diabetic Ketoacidosis (DKA)
Essential concept in the ED management of DKA: The focus is not on lowering the glucose, but rather closing the gap - Lorraine Lau & Winny Li
HWN Suggests
DKA Tips and Tricks
When looking at pH and bicarb, the differences between VBG and ABG are miniscule. For DKA patients, stick with the VBG as is less painful and has fewer complications.
LR is probably a better fluid for the large volume resuscitation required in DKA. Start with a 20 cc/kg bolus and then reassess the patient’s perfusion status.
Stay on top of your electrolyte repletion. If the patient has a working gut, you can aggressively replete potassium orally and don’t forget that when you are repleting potassium you also must replete magnesium.
Bolus dose insulin gets the patient to super-physiologic levels and has been associated with higher potassium requirements and more…
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Diabetic Ketoacidosis (DKA) Myths
I specifically covered four common myths that I still see people doing in regards to DKA management:
DKA Recognition and ED Management
Volume resuscitation must precede insulin therapy in order to adequately restore intravascular volume and tonicity. Early insulin therapy has the added risk of hypoglycemia and hypokalemia.
EM@3AM: Diabetic Ketoacidosis
Bicarbonate: Controversial, as the ADA recommends bicarbonate for patients with pH < 6.9. However, literature does not support this. To increase serum pH, the body has to blow off CO2, and in DKA, patients have maximized their ability to blow off CO2. Bicarbonate will lower serum K and result in intracellular acidosis, inhibit RBC oxygen release, and delay ketosis correction. Provide bicarbonate in patients in cardiac arrest and DKA, hyperkalemia with life-threatening dysrhythmia, and if in severe hemodynamic collapse.
Euglycemic DKA
Euglycemic DKA can occur in any diabetic, but there is a rising incidence in those taking SGLT2 inhibtors (-gliflozins). The pathophysiology behind this isn't totally clear yet though there are some theories.
Pediatric DKA: Don't Fear the Fluids
Why do we fear fluids in pediatric DKA patients? Do they really cause cerebral edema or is that just what you’ve been taught for years? Did you know that with each episode of DKA children lose some memory?
Articles of Interest
Euglycemia DKA – don’t miss it!
In Euglycemia DKA there is a “relative carbohydrate deficiency state with normalization of serum glucose and concomitant elevation of counter-regulatory stress hormones. This leads to free fatty acid catabolism and ketone production.” In any patient on a “zin” consider euglycemic DKA.
Basic Management of Diabetes…Not Just For Internists
We need to prevent our patients from spiraling into DKA or having an episode of life threatening hypoglycemia under our watch.
DKA and HHNS: One Kit Kat Too Many
The goal of fluids is to correct both hypovolemia and hyperosmolality. Most patients are profoundly dehydrated, and we administer rapid fluid boluses while awaiting further lab studies before starting insulin. Once fluid is running, correcting the sugar becomes the next priority, which is achieved with IV regular insulin at 0.1 units/kg/hr to tame glucose and close the anion gap. Be certain that the patient is not hypokalemic before giving insulin.
ED Management of DKA
IV insulin therapy should be started based on the anion gap, potassium level, and glucose level. When patients in DKA have potassium less than 3.3 mmol/L, potassium should be replaced prior to initiating insulin therapy as insulin administration will further lower extracellular potassium.
Hyperglycemia in the ED
DKA is a state of near absolute insulin deficiency. It typically occurs in Type 1 diabetics, but also occurs in type 2 diabetes under conditions of extreme stress such as serious infection, trauma, cardiovascular or other emergencies. DKA is more common in those <65 years old whereas HHS most commonly develops in individuals older than 65 years of age.
Review of Diabetic Ketoacidosis Management
Diabetic ketoacidosis (DKA) is a serious medical emergency caused by insulin deficiency that takes a significant toll on the U.S. healthcare system.
Resources
Core EM
Insulin should be held until the it is confirmed that the patient does not have severe hypokalemia to avoid resultant worsening hypokalemia with insulin infusion.
EMcrit Project
If unclear whether patient has DKA: beta-hydroxybutyrate & lactate levels.
WikEM
Patients in DKA are almost always K+ depleted despite initially fairly normal K+. This is due to extracellular shift of K+ due to acidosis as well as insulin infusion, which increases uptake of K+ intracellularly.

