Tweaking out on Sugar: Diabetic Ketoacidosis(DKA) vs Hyperglycemic Hyperosmolar Syndrome (HHS)

In this article, we’ll be discussing more about the complications associated with diabetes which I am sure many of you are familiar with; DKA and HHS. This is a follow up to the previous article where I talked about the basics of Diabetes.

Let’s take a look at some of the causes of DKA and HHS. Listed below are the 7 I’s (some literature list up to 8).

  1. Decreased amount of insulin

The rest of the causes listed below deal with increases in insulin demand:

2. Infections (UTI, cellulitis, pneumonia)

3. Intoxication (ETOH, Eric Clapton’s favorite drug cocaine, methamphetamines, etc)

4. Infarction (AMI, Stroke)

5. Inflammation (Cholecystitis and Pancreatitis)

6. Iatrogenic– This where we cause the issue which include wound healing from surgery and giving corticosteroids

7. Infant (Gestational diabetes)

If you are a long time viewer of our site, you know that I have this problem where I like to know WHY things happen and I have a tendency to nerd out a bit. NOTE: The following material may cause flashbacks to the wonderful time of college.

When there is a decreased amount of insulin in our bodies, it can cause some issues.

Insulin allows glucose to enter our cells. When there is a decreased amount of glucose, there will be a decreased amount of ATP production. When there is a decrease in the amount of ATP being produced, the body needs to get energy from our fat cells using a process called lipolysis which breaks down fat into fatty acids. These fatty acids undergo Beta oxidation which creates Acetyl COA. The Acetyl COA enters the Krebs Cycle and is then converted into ATP.

The Krebs Cycle can only handle so much Acetyl COA before it becomes overwhelmed. Therefore, the cells will use the Acetyl COA to create ketone bodies in a process called ketogenesis. As depicted in the picture above, one of the byproducts is acetone which we will discuss the importance of a little later. Now these ketone bodies will enter our blood and based off of their chemical formula, they have a high tendency to release Hydrogen ions. If you know a bit about Chemistry, the release of Hydrogen ions will cause a decrease in pH which will lead to acidosis, or more specifically ketoacidosis. Ketone bodies do a number of things which we will dive into. They can activate a region in the medulla oblongata called the chemo trigger zone to induce nausea and vomiting. They can also increase the anion gap. When patient’s have a high anion gap and acidosis, they have HAGMA (High Anion Gap Metabolic Acidosis). Now back to the hydrogen ions. Increased levels of Hydrogen ions in the extracellular fluid will cause our cells to respond by kicking potassium out of the cells which can lead to hyperkalemia; which will be one of the first killers in your DKA patient. This can cause chest pain, abdominal pain, and muscle weakness.

The increase in Hydrogen ions in our system can also stimulate our peripheral chemoreceptors. These chemoreceptors are like “whoa man! This is a lot of acid, let’s kick it out”. This causes an increase in respirations (Kussmaul respirations) which is meant to exhale CO2 in an effort to preserve the pH. As you can see, acetoacetate can be broken down into acetone which can be sent to our lungs and exhaled giving these patients the “fruity breath”.

The other 6 I’s which deal with an increase insulin demand can cause stress. Probably similar to that felt studying for the GRE.

When you are stressed, you will activate your sympathetic nervous system which releases catecholamines such as Epinephrine and Norepinephrine which increases glucagon levels. And if we are talking about glucagon, we will obviously be talking about the liver. Epinephrine, Norepinephrine, and glucagon cause Gluconeogenesis and Glycogenolysis in the liver (I’ll spare you the whole process) which will create our sugary friend glucose; and it will make a lot of it.

Now the whole point of the kidneys is to filter the blood and create urine. When there is a metric ton of sugar in your blood, it will try to secrete it. Water and sodium love to follow sugar around, just like the paparazzi, so the patient will have polyuria which can lead to dehydration (osmotic diuresis). Dehydration will lead to hypotension which leads to decreased renal perfusion, and decreased urine output. Decreased amounts of water with high levels of glucose is called hyperosmolarity. Our bodies love being at equilibrium and will do anything to achieve that to become comfortable. Because the blood is hyperosmolar (full of glucose and less water), our brains and cells will shunt water to the blood to equalize it. This leads to shrinking of the cells.

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When the cells shrink, it can cause AMS, weakness, seizures, coma, and eventually death.

DKA vs HHS

DKA

DKA is primarily seen in Type 1 diabetics. These patients will have Kussmaul respirations with the sometimes “fruity breath” caused by ketones. DKA primarily occurs fairly quickly.

Serum Glucose>250 mg/dL
pH<7.30
Bicarbonate (HCO3)<18 mEq/L
Anion Gap>12
Serum OsmolalityVariable
Urine/Serum KetonesPositive

Literature differs between what the serum glucose starts out at for DKA. Some say >250, >300, and >350 mg/dL so take it with a grain of salt.

HHS

HHS is primarily seen in Type 2 diabetics. HHS usually occurs after several days.

Serum Glucose>600 mg/dL
pH>7.30
Bicarbonate (HCO3)>18 mEq/L
Anion GapUsually <12 but can be variable
Serum Osmolality>320
Urine/Serum KetonesMostly Negative but can occur

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This site is meant to be used for educational use only. We strive to push evidence based medicine with no bias to help you obtain all the important information. You should always follow your protocols that have been set in place.

Scopeducation Team (Matt)

References

American Diabetes Association. (2004, January 1). Hyperglycemic Crises in Diabetes. Diabetes Care. https://care.diabetesjournals.org/content/27/suppl_1/s94.

Brubaker, R. H. (2021, April 1). High Anion Gap Metabolic Acidosis. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK448090/.

Chaudhry, S. (n.d.). Hyperglycemic emergencies: diabetic ketoacidosis and hyperosmolar hyperglycemia state. MPR | pathophys.org | beta. http://www.pathophys.org/hyperglycemic-emergencies-diabetic-ketoacidosis-and-hyperosmolar-hyperglycemia-state/.

Gosmanov, A. R. (2018, April 28). Diabetic Ketoacidosis. Endotext [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK279146/.

Hernandez, R. (2017, April 19). Does Fluid Choice Make Any Difference in DKA? blog.clinicalmonster.com. http://blog.clinicalmonster.com/2017/04/19/fluid-choice-make-difference-dka/.

Palicka, V. (2002, December 1). Pathophysiology of Diabetes Mellitus. EJIFCC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6195783/.

Pathophysiology of Diabetes Mellitus. Kindred Healthcare. (2013, November 7). https://www.kindredhealthcare.com/resources/blog-kindred-continuum/2013/11/07/pathophysiology-of-diabetes-mellitus.

Reading, J. (2016, July 5). ACTRAPID: Eight Steps For Managing Diabetic Ketoacidosis. Ausmed. https://www.ausmed.com.au/cpd/articles/managing-diabetic-ketoacidosis.

Schotola, H., Toischer, K., Popov, A. F., Renner, A., Schmitto, J. D., Gummert, J., Quintel, M., Bauer, M., Maier, L. S., & Sossalla, S. (2012, August 13). Mild metabolic acidosis impairs the β-adrenergic response in isolated human failing myocardium. Critical Care. https://ccforum.biomedcentral.com/articles/10.1186/cc11468.

Wantanabe, S., Hirakawa, A., Aoe, S., Fukuda, K., & Muneta, T. (2016, August 8). Basic Ketone Engine and Booster Glucose Engine for Energy Production. https://openventio.org/Volume2-Issue1/Basic-Ketone-Engine-and-Booster-Glucose-Engine-for-Energy-Production-DROJ-2-125.pdf.

Westerberg, D. P. (2013, March 1). Diabetic Ketoacidosis: Evaluation and Treatment. American Family Physician. https://www.aafp.org/afp/2013/0301/p337.html.

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