A Sweet DKA Review

In this post, we’ll take a look at a Hyperglycemic crisis and review Diabetic Ketoacidosis (DKA).  If you’ve worked in health care for any period of time, there are good odds that you have cared for a DKA patient. Beyond an elevated blood sugar, how well do you know what is really happening? Let’s take a look.

DKA is an acute, life-threatening complication of diabetes (typically Type 1). In Type 1 diabetes, there is a destruction of beta cells (insulin manufacturing plants) within the pancreas, therefore, preventing it from producing and secreting insulin. This results in these patients having a constant state of insulin deficiency. As long as the body doesn’t exceed its primary energy needs, most patients can maintain homeostasis. The problem lies when the body becomes stressed into a hyper-dynamic state, requiring the use of more energy. In this state, the body needs large amounts of nutrients. Our body typically contains plenty of these nutrients, but given their constant state of insulin deficiency, they are unable to process them for the energy they need. They start to become fatigued, which is one of the primary symptoms of DKA. This is typically where DKA takes root.

Once in this state of energy deficiency, our body starts to change the way it metabolizes the nutrients it does have access too. For this metabolism to take place, the role of insulin in fat storage becomes reversed, and enzyme hormone-sensitive lipase within the fat cell becomes strongly activated. Once activated, this causes hydrolysis of stored triglycerides, releasing large quantities of glycerol and fatty acids into circulating blood. Therefore, it increases the concentration of free fatty acids within the plasma. These free fatty acids now become the primary energy substrate for virtually all tissue, except the brain. The downside to the brain and all its complexities, it can only process two types of energy; glucose and ketones. Given the brain is “El Jefe” and has this energy preference, the body starts transforming all other forms of nutrients into glucose and ketones. 

This is where our liver comes into the equation. Proteolysis happens in the muscles and breaks down proteins into amino acids, and in adipose tissue, lipolysis breaks down the triglycerides within the lipids into free fatty acids and glycerol. The amino acids, free fatty acids, and glycerol are then transported via the bloodstream and into the liver. Once in the liver, gluconeogenesis takes place and converts it all into glucose. During this reaction, the byproduct acetyl CoA is created and goes through a process called ketogenesis to turn into ketones. The latter method is glycogenolysis, where glycogen is broke down into glucose. 

These patients are extremely sick, and when the previously stated hormone-sensitive lipase is strongly activated, and they dump all of their fatty acids into the blood. The concentration rises rapidly, and these patients can quickly worsen within hours and/or days. All of the processes we’ve discussed are complicated and cause the patient to present in multiple ways. During the process of lipolysis, a byproduct from the process is created in the form of cytokines. This causes inflammation and irritation to the GI tract. Typically they start with nausea, vomiting, abdominal pain, and present with cool-clammy skin. Eventually, they become severely dehydrated and have AMS, likely progressing to unconsciousness. 

But why the dehydration? This is an important concept. Sure, they may be undernourished and have possibly been actively vomiting, but keep in mind that what started this all is their insulin deficiency. All of this glucose that they’ve creating can’t be fully utilized and removed from their blood, and a vicious cycle begins and results in hyperglycemia. When the body is functioning appropriately, the kidneys are typically able to uptake the glucose while it filters the blood, but with the increased amounts of it now within the system, the kidneys are not able to process it all. This is when glucosuria occurs, and the glucose gets excreted in the urine. Given that glucose in the urine is an osmotically active solute, the urine sucks all of the water out of the bloodstream, causing severe dehydration with typically associated hypotension.

Finally, these patients will have a lower pH associated with their illness. This occurs because of the ketones we are producing for the body via ketogenesis. Remember, ketones are acids and are being delivered via mass production in our liver to help support the brain during this nutrient/energy-deficient state. The addition of these ketones lowers the pH, and because of the amount, the body’s buffer system can not keep up, ultimately causing metabolic acidosis. 

Hopefully, you are now able to appreciate the complexities involved in this process and have a better understanding of what makes this a vicious cycle for these patients, and why they can so rapidly spiral into a severe presentation. With that said, it is essential to do a full and meticulous history and examination of symptoms when treating diabetes patients. Remember, your care will be sub-par if your assessment is just that. 

 

*You can find more information on our After the Call podcast here.


Author

Josh_Headshot

Josh Piotrowski is an Active Flight Paramedic and Base Educator. He has over 15 years of experience, with the last six being focused on Critical Care Transport. Josh has spent his entire career focusing on being part of education, and the development of new employees and students. When Josh switched from inner-city Pre-Hospital EMS (PHEMS) to Critical Care Transports is when his passion for medicine intensified. Removing the traditional boundaries associated with PHEMS enabled him to find “calm in chaos,” and propel his studies of complex topics further than he ever imagined.


https://spectrum.diabetesjournals.org/content/15/1/28

https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-epidemiology-and-pathogenesis?topicRef=1795&source=see_link#H2

Guyton and Hall Textbook of Medical Physiology, 13th edition

Robbins Pathologic Basis of Disease, 6th edition

2 thoughts on “A Sweet DKA Review

Add yours

  1. This was very informative, thank-you. Would you consider a post going into more detail on HHNS vs DKA? Right now, in my mind HHNS is DKA without the coma. I’d like to be a little better versed.

    I think you meant “calm in chaos”? Unless “clam in chaos” is an expression the cook kids use?

Leave a Reply to Heavy Lies the Helmet Cancel reply

Up ↑