DKA
Diabetic ketoacidosis is the result of two problems: insulin deficiency and excessive release of counterregulatory stress hormones. Counterregulatory stress hormones include glucagon, cortisol, growth hormone, and catecholamines – they work to oppose the actions of insulin and increase the energy availability for the body (aka, gluconeogenesis and glycogenolysis). When the body is under extreme stress, these hormones drive up blood sugar levels. This, paired with a suboptimal insulin response, can lead to DKA.
While diabetic ketoacidosis is characteristically associated with Type 1 diabetes, it can be seen in Type 2 diabetics under conditions of extreme stress (such as serious infections, cardiovascular emergencies, or trauma). The triggers for DKA are easy to remember with the 5S rule:
Sepsis
Surgery
Sugars (missed insulin dose)
Stress
Substances (alcohol, drugs)
Symptoms of DKA include excessive thirst and urination, delirium/dizziness, dehydration, ketotic breath, and abdominal pain. And remember, just because the patient does have “diabetes” in their past medical history, doesn’t mean you should cross DKA/HHS off your differential. Diabetes can certainly remain undiagnosed if the patients isn’t following up with their PCP on a regular basis.
So, how do we diagnose DKA? The name says it all – glucose is elevated, pH is low, and ketones are up. However, there are actual diagnostic criteria – four to be exact. Fortunately, there is an easy acronym to remember these criteria as well: DKAA
D – diabetes (glucose must be >250 mg/dl)
K – ketonemia (measure with a UA and serum beta-hydroxybutyrate)
A – acidosis (pH must be <7.3)
A – anion gap (serum bicarb must be <18)
If your patient does not meet ALL four criteria, they do not have DKA.
The name says it all, but there are actual diagnostic criteria. Glucose is elevated, pH is low, and ketones are up. In treating, you need to correct the acidosis caused from generating all those ketone bodies generated from ketolysis due to the inability to burn glucose. Beta-hydroxybutyrate is actually the most common ketone body (there are multiple) with acetoacetate being less common. Acetoacetate (acetone) triggers the urine ketone test so it is possible to be in DKA with negative urine dip for ketones, but that would probably only be very early. For serum testing just go with beta-hydroxybutyrate serum levels if you can.
Beta-hydroxybutyrate is actually the most common ketone body (there are multiple) with acetoacetate being less common. Acetoacetate (acetone) triggers the urine ketone test so it is possible to be in DKA with negative urine dip for ketones, but that would probably only be very early. For serum testing just go with beta-hydroxybutyrate serum levels if you can.
The severity of DKA is determined by the pH since the glucose can be variable. This study showed that mild DKA could be treated with aspart subcutaneous insulin just as well as IV insulin. Of course, if the patient is exhibiting neurologic symptoms like AMS (drowsy/stupor), then their condition is more severe and potentially even life-threatening. Also, consider HHS if patient has an AMS and hyperglycemia but their pH is normal.
In treating, you need to correct the acidosis caused from the ketolysis that is a result of the body’s inability to utilize its glucose. Start with the following:
Isotonic fluid replacement – HYDRATE. HYDRATE. HYDRATE. These patients can have a water deficit of as 5-10L so don’t be shy with the IVF. It’s good to start with LR or PlasmaLyte because large amounts of NS (4-5L) can add free H+ to cause a hyperchloremic metabolic acidosis.
But wait! Make sure you check their electrolytes first, especially potassium. Patients in DKA typically have a substantial potassium deficit due to glucose-induced osmotic diuresis. However, their lab values usually don’t reflect that. In acidosis, the body tries to compensate by driving H+ into the cell in exchange for K+. Because of this, potassium can appear to be normal or falsely elevated at presentation. If their potassium is <3.3, make sure to replete before initiating fluids and insulin as this will drive potassium back into the cells.
Insulin at 0.1 units/kg/hr - stop drip when AG closes, might even need to continue when glucose <200 but add Dextrose (D5 or D10) to the fluids.
Potassium will fall: easiest rule to remember was discussed in the July 2017 EM:RAP episode as the 3.5 to 5.5 rule. If potassium is above 5.5, just start the insulin infusion, if between 3.5-5.5, add K (10-20 meq) to the fluids. If it is less than 3.5, hold the insulin, supplement the K and start the insulin later. Strictly speaking, according to more universal guidelines:
if K <3.3 replace K 30 min prior to insulin
if K 3.3-5.0 replace K during insulin drip
Phos replacement if below 1mg/dL
Mg replacement if low or symptomatic
Bicarb not recommended
Monitor the patient's mental status, respirations, AG, glucose, bicarb, and K closely, usually every hour initially. Remember, you're not done when you start the insulin drip. These are ICU patient's that need one-to-one nursing with at least q1hr glucose/lab checks.
Points to remember:
DKA Triad - hyperglycemia, anion gap metabolic acidosis, and ketonemia (look for beta-hydroxybutyrate)
DKA can be precipitated by noncompliance with insulin, trauma, infection, pregnancy, and other stressors and occurs in type I or type II DM. Look for, and correct, the precipitating cause, which might just be diet/med noncompliance.
Treatment: correct fluid deficit, acid-base disturbance, and electrolyte imbalance, administer insulin, and treat the underlying cause
