Breaking Down DKA (Diabetic Ketoacidosis) With NurseMike

January 8, 2017

Look, it's 2017 and we all know that Diabetes Type II is WAY out of control, like 29 million people (9.3% of U.S. population) out of control (1). The crux of it all is that the majority of Type II Diabetes cases are preventable! According to the Harvard School of Public Health, 9 out of 10 cases could be avoided by keeping the weight in check, getting out and exercising more, eating better and putting down the ciagarettes (2).

 

 

Looking at the statistics, it doesn't look like anybody's getting it, and unfortunately this is why we are beginning to see more and more illnesses resulting from diabetes in the hospitals these days. For all of the non-medical readers out there you should know that diabetes can cause heart disease and increased risk of death from heart disease and stroke, nerve damage, foot problems, skin

 

complications, dental disease, kidney disease and eventually kidney failure (which is a whole new set of serious circumstances) AND is the number one cause of blindness (3).

 

 One of the most complex disease processes associated with diabetes is a little something called Diabetic Ketoacidosis (DKA). It's so complex because of the multiple hormonal abnormalities and electrolyte imbalances that are going on within the body that can continue to spiral out of control and eventually lead to coma and death if not corrected (4). In people with diabetes, DKA is commonly triggered by a number of things, but mostly physical or emotional trauma, heart attack, alcohol or drug abuse, particularly cocaine, certain medications, such as corticosteroids and some diuretics (5).

 

If you're new to nursing and you work in the hospital setting, this post is for YOU! At the rate that diabetes is growing, you will MOST CERTAINLY come across DKA and its important that you get this. Unfortunately, not ALL hospitals have the same protocols (I'd love to know why), but if you understand the pathology it'll help you as you treat patients going through this horrible disease process no matter what hospital protocol you're following. Not to mention you'll feel like a rockstar when you get this down while everybody else is looking this stuff up. Alright, let's get to work!

 

Pathogenesis

 

Your pancreas has ALPHA cells and BETA cells (also has Islets of Langerhans but not pertinent right now). Alpha cells produce the hormone glucagon and your BETA cells produce the hormone insulin. Insulin is responsible for shuttling sugar floating around in your bloodstream into the cells of your body to be used to make energy AND inhibits lipolysis. If there's no insulin OR your body is less sensitive to your insulin cells than they used to be, problems result from too much sugar in the blood. 

 

Glucagon on the other hand is responsible for raising blood sugar by increasing glucose production in the absence of sugar OR insulin and also promotes ketogenesis . Did you catch that? I hope you did. Reread it again just in case. If there's no insulin or the body is insensitive to it's own insulin that means that the body's cells are starving for sugar in order to make energy. This causes the Alpha cells to release glucagon to break down fat (lipolysis) in order to free up some fatty acids the body will use to make ketone bodies to use for energy. If you're into bodybuilding you may have gone "ketogenic" before in order to drop weight quickly. This is where you stay away from carbs so that your body will use fat stores for energy production. YOU CAN GET SHREDDED!

 

Anyway, I digress. This gets REALLY technical for a few seconds so pay VERY CLOSE ATTENTION to this next part...

 

Glucagon (released from Alpha Cells when cells need sugar and insulin isn't doing the job) in the bloodstream increases mitochondrial uptake of Free Fatty Acids (FFA) (increased amount of FFAs floating around in the blood stream because of the actual or perceived lack of insulin and release of glucagon, causing lipolysis) by decreasing Malonyl Coenzyme A (CoA) while increasing hepatic carnitine sooo....

 

-CoA usually prevents oxidation of FFAs. So without CoA oxidation of FFAs occur to produce more substrate for ketogenesis to occur.

 

-Because of the lack of insulin lipolysis is happening A LOT. The increased amount of FFAs entering the mitochondria and the Citric Acid Cycle (KREBS Cycle) overwhelms the mitochondria's ability to convert FFAs to energy. This is what causes increased ketone bodies (acetoacetic acid and B-hydroxybutyric acid) floating around in the bloodstream (hyperketonemia). 

 

-Once the body's natural buffering systems aren't doing the job systemic acidosis hits. Have you ever smelled someone's breath who is going through DKA? It's smells fruity. This smell is from the keto acid acetoacetic acid that's been converted to acetone and expelled through the lungs.

 

Insulin and glucagon aren't the only hormones that play a role in DKA. You're also dealing with the stress hormones cortisol, epinephrine and growth hormone (6).

 

-These stress hormones are lipolytic, further contributing to the increased FFAs floating around in the bloodstream, overwhelming the mitochondria resulting in increased ketone acids building up.

 

-In addition to being lipolytic they also promote protein breakdown by communicating to myocytes that we need energy (6)!

-This muscle breakdown allows gluconeogenesis  (conversion of protein to glucose) to occur, further increasing circulating blood glucose and hyperosmolarity of the blood stream and further electrolyte imbalances causing the 3 Ps you've probably already heard of (polydipsia, polyuria, polyphagia).

 

So what's this looks like?

 

At this point the patient is VERY critically ill resulting from dehydration, hyperosmolarity, electrolyte abnormalities and acidemia. The blood glucose doesn't have to be very high to be in DKA, especially if this is a new condition for the patient. I would expect a blood sugar result greater than 250mg/dl but have seen it as high as 1100mg/dl (70-100 mg/dl is normal). The patient is most likely very lethargic if not seemingly comatose, they are breathing really fast (body trying to lower acidity level by blowing off keto acids), their heart rate is most likely very rapid greater than 100, their skin may also be very dry and/or very pale and they may have ongoing tremors (7).

 

Lab data to monitor:

Blood Sugar

ABG

Urinalysis (ketones present)

Lactic Acid

Anion Gap 

    = Anion Gap=[Sodium (mEq/L) + Potassium (mEq/L)] - [Chloride (mEq/L) + HCO- (mEq/L)]

Potassium

 

How are we to treat it?

 

When I was a rookie, my thinking was we need to get this sugar down and get it down as fast as we can. Although I was partially right, we do need to get the sugar down, we could do some serious damage if we bring it down TOO fast. Also, bringing the sugar down is only part of the problem. We have all these metabolic and electrolyte derangements we need to address while we're attempting to bring the sugar down. So how do we treat this thing? The answer is STRATEGICALLY. Let's tackle this thing step by step.

1st-Fluid Replacement: Remember the patient is extremely dehydrated. It could have even been what caused this whole mess in the first place. We must rehydrate. According to Medscape (7) you can expect the first 1-5L to be isotonic sodium chloride soluion (NS) or lactated ringers solution (LR). Once the patient is well-hydrated you can expect the fluids to change to a 1/2 NS, especially if hypernatremia (high sodium) is an issue. Once blood sugar levels reach around 180 mg/dl look for the clinician or protocol to change fluids to 5%-10% Dextrose (most likely 5%).

 

*p.s.-if the patient is severely dehydrated you could look for the clinician to change fluids to Normosol or something similar where the chloride is replaced with acetate in order to prevent hyperchloremia acidosis (way too much chloride in the blood).

 

2nd-Insulin-Insulin therapy is a little tricky. Because of dehydration, subcutaneous insulin won't do the job. IV insulin is called for here. This means hourly blood sugar checks. Sometimes the blood sugar will be so high your glucometer won't even be able to give you a numerical reading. In this case you'll have to send a sample to the lab every hour. When lowering blood sugar, you don't want to lower it too quickly due to the risk of causing c

 

erebral edema or neurological dysfunction (4). The optimal level of blood sugar decline is 100mg/dl/hr (7). Furthermore, because insulin administration causes intravascular potassium to be transported into the cell, it's important to be aware of the potassium levels, as well as other electrolyte levels...which brings me to number 3.

 

3rd-Electrolyte Replacement-Hypokalemia is the most common electrolye abnormality in DKA. The reason is because DKA causes total body potassium depletion by a few different mechanisms. First, the metabolic acidosis from ketoacidosis causes potassium to shift to the extracellular space. Second, due to the hyperglycemia and the glucosuria the the patient is voiding a lot and potassium is being excreted through the kidneys. Third, the patient has probably vomited a bit and potassium is always lost through vomiting.

 

If potassium levels are low potassium replacement should be started at the beginning. Look for the clinician or protocol to add 20-40 mEq/l of potassium chloride to each liter of fluid until corrected (7). You must be monitoring the potassium levels frequently at this point. It's suggested not to start insulin therapy until the correction of the potassium is underway. Mostly because Insulin drives potassium into the cell, which could further lessen the amount of potassium floating around the bloodstream, causing lethal cardiac arrhythmias. 

 

4th-Correction of Acid-Base Balance-Typically you won't have to worry too much about the acid-base balance with sodium bicarb. The body typically corrects itself if the above treatment is performed well. Also, it's been shown to cause worsening of hypokalemia if acidosis is corrected to fast. Sodium Bicarb has also been shown to cause cerebral edema in pediatric cases of DKA. 

 

*See this article on pediatric cerebral edema associated with DKA treatment

 

Diagnostics

Hourly capillary blood sugar checks-monitors glucose levels

Every four hour Chemistry Panels-monitors electrolytes, anion gap (3-11)

Every four hour ABGs-monitors lactic acid, pH

 

Navigating the waters of DKA can be confusing and difficult the first few times your exposed to it, but understanding the underlying pathology will really provide you a lot of clarity. As you're caring for these patients, many of them maybe experiencing DKA for the first time (8). This means they may not only be really sick, but really frightened and unsure also. Explaining what your doing and why you're doing it can go a long way in helping patients cope with what's happening to them while in the hospital and help you to understand and retain all that you've learned in treating DKA.

 

I hope this #BreakingItDown series has been informative and helpful to all you rock stars out there. I sincerely admire each of you for working as hard as you have to get this far and still continue to better yourselves by being a lifelong student studying your craft so you can take the very best care of your patients. People might not ever remember what you've said, but they'll always remember how you made them feel.

 

Thanks again!

 

#NurseMike

 

 

 

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References

1. https://www.cdc.gov/features/diabetesfactsheet/

 

2. https://www.hsph.harvard.edu/nutritionsource/diabetes-prevention/preventing-diabetes-full-story/

 

 

3. https://www.health.ny.gov/diseases/conditions/diabetes/problems_caused_by_diabetes.htm

 

4. Nathan, D. M., Buse, J. B., Davidson, M. B., Ferrannini, E., Holman, R. R., Sherwin, R., & Zinman, B. (2009). Medical management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy a consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes care, 32(1), 193-203.

 

5. http://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/basics/definition/con-20026470

 

6. Kerl, M. E. (2001). Diabetic ketoacidosis: pathophysiology and clinical and laboratory presentation. Compendium, 23(3), 220-8.

 

7. http://emedicine.medscape.com/article/118361-treatment#d8

 

8. http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html?referrer=https://www.google.com/

 

 

 

 

 

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