6 Ways To Lose DKA Style Points

I think most clinicians enjoy getting as much information as possible before getting on scene. It gives your mind time to start working through various scenarios, cross-check guidelines, and develop a game plan with your partner. I want you to read the following dispatch information and let your brain do a little premature future-telling.

Patients with diabetic ketoacidosis (DKA) are in a dynamic metabolic derangement that requires thinking multiple steps ahead, pre-planning, and exquisite attention to detail. If, upon receiving the dispatch information, you started to worry about the referring facility intubating a patient in a severe metabolic acidosis, we are exactly on the same page.

My partner and I started discussing the game plan, and I went through my mental checklist of "ways we lose style points on a DKA transfer."

Intubating purely due to mental status changes: A patient in severe DKA is typically exhausted, slow to respond, and sometimes even unresponsive. The good news is they turn around pretty quickly with fluids and insulin. The problem is that we are not used to seeing patients in that state, and not feel a push to take their airway. However, the brain is pretty damn smart and if the patient has adequate respiratory compensation and their airway is not in imminent harm, allowing them to maintain spontaenous negative pressure breathing is optimal.

Dropping glucose too quick: When you come across your first DKA in the field and see their glucose is 500 mg/dl, there may be a bit of an urgency to get that glucose back to normal. However, in DKA, the elevated glucose is really just a distraction. The problem isn't that the glucose is too high, it's that the cells can't use it because of an insulin deficiency. This can be corrected with insulin, but you have to be careful with the amount of insulin administered over a specific time. When a patient's blood sugar elevates it pulls fluid into the vasculature from the interstitial space. If the glucose is then rapidly corrected, the fluid will rapidly leak back out of the vessels. This is concerning for areas of the body that tightly regulate third spacing due to limited ability to expand, such as the brain. The concern is that a sudden change in serum osmolality can cause fluid to leak out of thr vessels and cause cerebral edema.

Starting insulin when the potassium is low or normal: Potassium concentration is way higher in the cells compared to the serum.

As the cells are forced to burn alternative fuel sources, the byproduct is various types of ketones. The ketones create an acidotic environment and increase cellular permeability, causing potassium to leak out of the cell and into the serum. If you were to stop at this point, you may assume the patient would become hyperkalemic.

However, we know that all that extra fluid that we pulled into the vessels is going to have the patient urinating quite often. This means that as long as the patient has functioning kidneys, they will urinate out that potassium into the toilet (or wherever). As soon as you start insulin, you begin shifting the glucose AND potassium into the cell. If not replenished, potassium levels can hit critical lows and cause fatal arrhythmias. This is why it is so important to ensure that you are replacing the potassium when administering insulin, even if the range is within normal limits. The body has to replenish the intracellular potassium concentration that it pulled from first before allowing serum levels to return to normal. This is further complicated if the patient is deficient in magnesium.

Not taking potassium with you (just in case): Nothing is worse than having to stop your insulin in transport due to your point-of-care lab draw showing the patient is hypokalemic. Most programs do not carry potassium. Therefore, most of us are in the habit of asking for it before we leave the referring. We did a podcast awhile back called "Don't stop the insulin."

In the episode we discussed how the insulin and volume resuscitation is what turns these patients around, and how it sucks when you are forced to stop the insulin because you failed to predict the need for potassium replacement.

Potassium replacement can come in various forms. If the potassium levels are not critically low, oral potassium is commonly preferred because of its slow and steady absorption rate and lack of patient discomfort. However, if potassium levels are critically low, IV potassium will get in the system faster.

While not on the initial list I made, I think it is important to mention briefly magnesium's critical role in potassium regulation. The renal outer-medullary potassium channel tightly regulates potassium excretion. When magnesium levels are low, nothing limits the outflow of potassium, as illustrated below. If you are replacing potassium and not paying attention to the magnesium levels, you will find yourself wondering why, despite potassium replacement, the patient remains hypokalemic.

Failing to address respiratory compensation: Why do patients in metabolic acidosis have to blow off so much CO2? It all comes down to how tightly the body regulates the CO2 floating around in the plasma. The majority of CO2 is transported as bicarbonate, and when ketones are stacked onto the anion column, the body has to dissociate bicarbonate into CO2 and water to maintain electrical neutrality. Lower serum bicarbonate levels equal a decreased threshold for CO2 in its dissolved gas form.

This is explained in detail in my blog "Kussmaul Logic."

The net result is that a patient sometimes pulls minute volumes as high as 20 lpm and maintains a PaCO2 level in the teens. This can be extremely hard to replicate after switching to positive pressure ventilation, which is why doing so is taken with great caution and an understanding of clear alveolar minute volume goals. The lower the bicarb is, the higher the alveolar minute volume needs to be. I say alveolar minute volume because while increasing rate alone can hit target minute volumes, it is at the cost of alveolar ventilation. Optimize tidal volume first and then increase the rate. If increasing the rates starts reducing your exhaled tidal volumes (VTE), optimize your I:E to ensure the inspiratory phase is not getting cut short and that you're not air trapping. The example below is for a male patient who is 5 feet 11 inches tall.

Volume resuscitation with 0.9% normal saline: I'll start by saying that if 0.9% normal saline is all you have on the truck and this is a 911 call, it is better to use normal saline than not to fluid resuscitate at all. DKA patients are typically dry, and fluid replacement is essential to DKA resuscitation. It is best to avoid 0.9% saline due to the chloride load. 0.9% saline has equal parts sodium and chloride (154 meq/L), which is way higher than the body's serum chloride. This causes the bicarbonate to shrink even more than it did for the ketones to make room for the chloride load.

The net result of fluid resuscitation aggressively with 0.9% saline is known as a "hyperchloremic acidosis." Once you get rid of the ketones in DKA, the serum bicarbonate level will return to normal. However, if you have introduced an abnormal chloride load with the fluid you chose to resuscitate, it will take longer to return to normal due to the chloride taking up more of the allotted anion space. This is why a more balanced solution, such as Ringer's Lactate or PlasmaLyte, is preferred.

Wrong Moves

I was talking with a new flight clinician at Life Link III the other day about approaching a complicated resuscitation. One of the things I mentioned that helped me formulate a game plan is to say, "What would the wrong move be here?" Instantly, your brain starts to identify why starting dopamine on a tachycardic septic patient would be the wrong move. Why delaying epinephrine in anaphylactic shock because you "just aren't sure" would be the wrong move. I think this does some psychological framing that makes the right moves stand out clear.

With as many moving parts as there are in a DKA resuscitation, pre-planning and having a strong mental model of the underlying physiology can really help ensure a smooth and purposeful resuscitation. This list is just a few things that came to my mind and is definitely not all-encompassing. I would love to know what your personal list looks like.

For more information, check out the "Advanced Metabolic Acidosis Ventilation" class in FOAMfrat Studio.

References

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