Endocrine Emergencies Part 1: DKA
What is DKA?
when your bodies insulin requirement acutely exceeds your bodies insulin availability - “anytime your body needs more insulin than your body got”
1) For patients who are on insulin: any interruption in insulin delivery
be careful to label patients “non-compliant”
2) Reduction in insulin sensitivity; proceeded by systemic stress (i.e. MI, pregnancy, infection)
can also be presenting diagnosis of diabetes
Acute insulin imbalance sends the body into a state of catabolism
Carbs – STOPs using glucose as energy source, START breaking down glycogen, leading to Hyperglycemia
Protein – STOP protein synthesis. START converting protein into glucose, leading to Hyperglycemia
Fats – Starts using fat as energy source through lipolysis and a catabolic process called beta oxidation. Essentially chopping carbons off fatty acid chains and using them as Kreb’s cycle intermediates.
Here’s the problem: there’s SO MUCH energy in fatty acids, that the body doesn’t have enough Kreb’s cycle enzymes to deal with it all. So as you’re chopping up fat, the excess carbons are converted into ketone bodies; In small quantities - NBD – can still be used as energy (particularly by the heart/brain). But in large quantities (as we see in DKA), this is where we develop the ketosis and acidosis
Three ketone bodies
Beta-hydroxybutyrate, acetoacetate, acetone
Presentation
Triad: Hyperglycemia, ketosis, acidosis (Quartetet/Tetrad? add hyperosomolar state)
The hyperglycemia (and even to an extent the ketone bodies) are osmotically active. Meaning, they concentrate the bloodstream and pull water out of our body cells
As the glucose and ketones make their way into the urine, water follows. LARGE volumes of urine – process called osmotic diuresis. This leads to severe dehydration, hypovolemia, and electrolyte loss (particularly potassium)
Smell – fruity odor
Dehydration and hypovolemia
Dehydration – loss of total body water.
By extension – means that the body is becoming MORE CONCENTRATED
Dehydration manifestations: poor skin turgor, dry mm, and particularly hypernatremia
Hypovolemia – loss of intravascular volume. Essentially a reduction in mean systemic filling pressure and preload
Hypovolemia manifestations: tachycardia, hypotension, and signs of hypoperfusion
THESE ELEMENTS ALMOST ALWAYS co-exist in DKA. The treatment for dehydration and hypovolemia are NOT the same
Kussmauls respirations: FAST and DEEP breathing
Meant to compensate for acidosis
Severe abdominal pain, nausea, vomiting
Mediated by prostaglandin
Be mindful of this one; symptoms sometimes concern you for an acute abdomen
NOT EVERYONE NEEDS AN ABDOMINAL CT. We recommend considering CT:
In patients with severe abdominal pain and only mild ketoacidosis, get a CT.
In the absence of this – follow serial abdominal examinations and treat the DKA. If worsening or unresolved, get a CT.
Altered mental status
Sort of the same problem; DKA can cause altered mental status, particularly in patients with severe hyperosmolality. But, you could also have a primary neurology process like meningitis that is driving the DKA
NOT EVERYONE NEEDS A CT HEAD OR LP.
Consider neurologic workup in patients with AMS and normal serum osm
In the absence of this – follow serial neurologic examinations and treat the DKA. If worsening or unresolved, get a CT
Treatment
We advocate for a three-pronged treatment approach that considered fluid status, electrolytes, and insulin (in that order)
Fluid status
Remember these patients are often both hypovolemic and dehydrated - accordingly, begin by assessing the patient’s intravascular volume status
Exam – feel their skin, pulse amplitude (I often put my hand on the radial pulse – can do both at once), cap refill, neck veins
Heart rate, blood pressure (usually tachycardic, not often hypotensive anecdotally)
Ultrasound – IVC assessment. Or – even just fluid challenge; give a liter of crystalloid and reassess; 9 times/10, patient is going to need a good bit of fluid
2-3L and stop, reassess after that.
Next, assess the patient’s hydration status – remember, this is an assessment of TOTAL BODY WATER
Exam – mucous membranes, skin turgor (though these techniques have questionable likelihood ratios in isolation)
Patients with dehydration almost invariably present with hypernatremia
We need to use the corrected sodium calculation (MDCALC)
When there is confirmed dehydration, you’ll want to give a HYPOTONIC FLUID
Hypovolemia is treated with crystalloid
Dehydration is treated with hypotonic fluid like 1/2 NS
Electrolytes (Na and K)
But the big electrolyte to pay attention to here is potassium
In terms of total body potassium, almost all patients with DKA have severe whole-body hypokalemia; HOWEVER The acidosis causes shifting of potassium FROM the intracellular space and TO the bloodstream
THIS MEANS
Even though the patient may present with hyperkalemia their true potassium level is actually QUITE LOW
DO NOT treat hyperkalemia if it’s present. Treatment of the DKA WILL resolve this electrolyte abnormality
If anyone with DKA presents with HYPOkalemia, their TRUE potassium is actually WAAAY lower
If the potassium is less that 3.3 mEq/L, DO NOT START INSULIN
Aggressively replace K, then recheck; This can be unsettling for some, especially if the pH is remarkably low
It is MUCH BETTER for a patient to sit with severe acidosis due to DKA while you fix the potassium, than it is to try and treat the DKA and end up with hypokalemic VF
If the potassium is greater than 5 mEq/L, start insulin and rest easy
The K will normalize, you might need to replace at some point in the patient’s treatment course
If the potassium is between 3.3 and 5.0 mEq/L
Consider a maintenance infusion with potassium
Insulin
We know we need to address the patient’s perfusion and volume status, and we know that we need to assess the potassium before we can safely administer insulin. Once those things have been done, then and only then can we start our insulin therapy
Usually – 0.1u/kg bolus followed by 0.1u/kg/hr (recommended dosage from most major endocrine societies)
Most hospitals have their own protocol
Key here – NOT targeting a specific glucose “level”
You want to get the body out of its catabolic state (stop generating ketones)
Accordingly, your target is “closing the gap”. This means – patient may develop hypoglycemia before the gap is closed
Usually what we’ll do is continue the insulin gtt and switch to dextrose containing maintenance fluids (D5, D5 NS, D5 ½ NS) when the glucose level is less than 250 mg/dL
PEARLS
NEVER-DO’s
Correct hyperkalemia (ad-lib)
Give bicarb (ad-lib); use insulin bolus instead
Intubate (ad-lib); consider bipap; if you intubate, use pressure support
When to transition
When it’s ok:
Gap is closed, Hyperglycemia improved, Acidemia improved, Tolerating PO
How to do it
Give intermiediate or long acting insulin
Continue insulin drip for 1-2 hours
Continue chosen insulin dosing regimen
Insulin dosing regimens
Resume home regimen (Why or why not)
Calculate 24 hour insulin req – 50% basal and 50% prandial
0.25-0.5U/Kg/Day, 50% basal, 50% prandial
There are 100 ways to do it, most of them are going to require titration, and, if it’s new insulin script, need to make sure patient can afford/access
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