 Welcome to Nursing School Explained. Today's topic is diabetic ketoacidosis or DKA. It mostly affects type 1 diabetics and if you haven't already done so, please watch my video on the comparison of type 1 and type 2 diabetes. DKA is a complication that is associated with type 1 diabetics. So let's look at the causes. There are basically three different causes which can be missed insulin dosages, inadequate insulin because the patient is under a lot of stress or has an active infection, or they are newly diagnosed type 1 diabetics. So sometimes the patient will not know that they are diabetic. All these pathophysiological mechanisms will kick in and the patient will end up in DKA at the hospital and then it will be discovered that he or she is a type 1 diabetic. So in order to really understand how this happens, let's look at the pathophysiology. So usually our body needs insulin to break down glucose for metabolism and the insulin allows the glucose to enter the cells so it can be taken up. Any additional glucose that's not being used for cellular metabolism right away is stored in the liver as glycogen and available later on in case of an emergency when there might not be enough glucose available. Certain mechanisms will kick in and release that glycogen back from the liver and we'll go into that here. So now in diabetic ketoacidosis there's inadequate insulin for normal cellular metabolism because we just cannot absorb it. So then the body says wait a minute I need some energy stores, my cells are starving so it's going to break down fat stores for energy and the liver converts these fatty acids into ketones and you might have heard about the keto diet or ketoacidosis which is basically banking on this kind of physiological principle to eat up fat stores for energy rather than glucose that's normally our primary source of energy. So these ketones that are now being broken down, they have a very low pH and whenever we're dealing with low pH we have to worry about the body becoming acidic. So that will lead to metabolic acidosis and the reason here is that it is stemming from the renal system and again acidosis a pH less than 7.35. Now in addition to this breakdown of the fatty acids there are two more principles that happen here. So in addition the alpha cells from the pancreas now release glucagon which combines with the glycogen stores from the liver that the body has stored originally after the glucose was absorbed leading to this principle called gluconeogenesis. So it's basically a backup mechanism where if there was periods of starvation for example and we would not be able to consume some source of glucose or fast energy it's a built-in mechanism that we have where the pancreas and liver can combine these two enzymes and then release an alternative store of energy that the body can use. And number two the adrenal glands release cortisol which leads to glycogenolysis and both of these mechanisms in addition to these ketones were already broken down will lead to extremely high levels of blood sugar and with that the blood becomes very thick and saturated which leads to hyperosmolarity that's basically the concentration of the blood in comparison to its solutes which then leads to osmotic diuresis. And osmotic diuresis is something that happens when there's increased osmotic pressure at the renal tubules and now these renal tubules are unable to reabsorb water and sodium leading to as we'll come to see the signs and symptoms here in a moment. So basically there's lack of insulin, the cells are starving because they have no source of glucose because the insulin is needed to break down the glucose and bring it into the cells so the cells can use it, fatty acids are broken down, ketones leading to acidosis in addition the cells are still starving and the alpha cells from the pancreas and the glycogen from the liver combine with the cortisol leading to extremely high blood sugar levels causing all these osmotic pressure and then eventually dehydration. So let's look over here at signs and symptoms. So we have the three P's which is polyuria, polydipsia and polyphasia. So if the patient has this osmotic diuresis the body is going to try to get rid of some of this fluid and we cannot really reabsorb any sodium and water therefore this diuresis will happen making the patient very dehydrated. In addition the patient will be very thirsty because now they are urinating frequently getting rid of some volume therefore the thirst mechanism will kick in and patients will be very thirsty and then also they'll be very hungry polyphasia because we don't have any glucose to be using we're using fatty acids for breakdown therefore the body will be starving and patients will be hungry so polyuria, polydipsia and polyphasia. In addition this osmotic diuresis and the inability of the renal tubules to reabsorb sodium and water will lead to significant dehydration which in turn will lead to hypovolemia so the patient will be very dehydrated evidenced by low blood pressure and increase in heart rate. And then initially potassium levels will be elevated. So potassium is typically a intracellular electrolyte but now we have all this hydrogen which is basically all the acids from these ketones that are floating around in the serum and the body moves the hydrogen from the serum because it's so acidic into the cell but something has to come out of the cell and that will be the potassium and we know that elevated potassium or any kind of potassium imbalance will put the patient at risk for dysrhythmia. Now later when this osmotic diuresis kicks in and we have in trouble reabsorbing the sodium, the water and the potassium, the potassium level can actually get a little bit lower, so hypocholinea. Patient because they're acidotic they will have kuzmol respirations and those are probably some of the basic breath patterns that you've learned about. It'll be a very, almost like an erratic fast breath. It'll sound something like that. It'll be this kind of pattern because the patient is acidotic and the respiratory and renal system work together to maintain homeostasis in terms of pH level so now if there's something going on from a metabolic standpoint the respiratory system will try and get rid of some of the CO2 which is an acid to blow that off to maintain homeostasis and bring the pH back into normal level. Now in addition patient will have acetone breath which is also described as a fruity breath because those are the key tones that are building up that we can smell. Patients a lot of times are nauseated or vomiting and they can be very lethargic because they are dehydrated and there's all these electrolyte imbalances that can be going on and eventually it can lead to coma so patients can die from diabetic ketoacidosis. Now DKA is diagnosed usually by a blood sugar level that's greater than 250. Positive key tones in the urine so that's basically being spilled over, not filtered by the kidney and then a pH less than 7.30 and a bicarbonate level of less than 18 which basically these two in combination just tell us that there is metabolic acidosis going on. Now how do we treat that? So first things first we need to correct the dehydration and the hyperbolemia that we said over here so isotonic IV fluids and patients might require large amounts of that so 2-3 liters of normal saline is not unheard of over a very short period of time as well as insulin so because we have no insulin available we need to supply the patient with IV insulin. Keep in mind that the only insulin that you can administer intravenously is a regular insulin so you can never administer any type of other insulin other than a regular. And then we're going to have to correct electrolyte imbalances. Now most of the time when the patient's illishly hyperkalemic once we control the isotonic IV fluids, once we administer that and control the patient's hyperbolemia as well as give them insulin so now this mechanism is basically negated so now the homeostasis of normal metabolism is reestablished because we're now supplying the insulin so the body can use all that blood sugar that's circulating in their bloodstream. The electrolytes will balance themselves out because now we're less acidic that hydrogen iron moves back out of the cell into the extracellular fluid and the potassium can move back into the cell where it belongs automatically correcting the electrolyte imbalance. So patients with DKA a lot of times end up in the intensive care unit because they're critically ill because of this metabolic acidosis that's happening. It can be corrected fairly quickly but also after the diagnosis of DKA if this was a patient who was newly diagnosed with diabetes or maybe who was an uncontrolled diabetic or has not received adequate education on how to manage their diabetes during periods of stress or infection there are going to need a lot of education and nursing care to be able to manage the diabetes better so that they won't suffer from this complication again. Thank you for watching this video. Please share, subscribe and also follow my Instagram at nursing school explain to keep up to date with the newest release of videos. Also see my video on diabetes type 1 and 2 as well as HHS which is the complication of type 2 diabetes. Thanks for watching. See you next time.