Diabetic Ketoacidosis (DKA)

hello i'm eric from strong medicine in today's episode of intern crash course i'm discussing diabetic ketoacidosis better known by the acronym dka there are three key features of dka hyperglycemia compounds called ketone bodies in the blood a state known as ketonemia and an elevated anion gap metabolic acidosis there's an asterisk next to the hypoglycemia because there are cases of eu glycemic dka in which the blood sugar is either normal or near normal although this is a rare occurrence awareness of this phenomenon has increased in recent years on account of it being a side effect of the sglt2 inhibitor class of diabetes and heart failure medication dka has overlapping symptoms and pathophysiology with another hyperglycemia crisis called the hyperosmolar hyperglycemic state or hhs although these two conditions can co-exist they usually don't let's take a look at the similarities and differences in their clinical features as already mentioned the hallmark features of dka are hypoglycemia ketonemia and acidosis while the hallmark features of hhs are hyperglycemia and hyperosmolarity in both cases the hyperglycemia leads to polyuria and dehydration in dka the ketonemia and acidosis lead to dyspnea which is usually on account of respiratory compensation for the metabolic acidosis a distinctive but easily overlooked breathing pattern that is known as cousmal respirations is sometimes observed in dka in which the patient has a normal or near normal respiratory rate but with a very increased tidal volume resulting in an increased minute ventilation why this pattern is anecdotally seen more with dka than in other forms of acidemia is not known in addition the ketonemia and acidosis of dka are also commonly observed to cause abdominal pain though the mechanism for this is also not clearly established meanwhile with hhs the hyperosmolarity leads to confusion and somnolence in cases where dka is associated with significant hyperosmolarity and altered mentation it may be appropriate to state that both dka and hhs are present simultaneously on the other hand if a person with dka is confused or somnolent but serum osmolarity is normal or near normal the alternation is likely due to the acidemia or dehydration and claiming the presence of hhs would be incorrect because dka and hhs are sometimes confused for one another i'll continue the comparisons for another minute the degree of hyperglycemia in dka is usually lower than in hhs looking at the epidemiology dka is typically seen under the age of 65 is relatively common and most patients have type 1 diabetes though a significant minority have type 2. hhs on the other hand is the opposite of these the volume deficit which is a decrease in total body water and salt in dka is moderate to severe while in hhs it is almost always severe the free water deficit which is dehydration in excess of the decrease in solute in dka is none to mild while in hhs it is always present and always severe regarding the arterial ph in dka it's low while it's usually normal in hhs concurrent metabolic derangements are virtually always present in both but they are not the same in dka derangements of potassium are usually the most clinically relevant largely due to the transmembrane shifts driven by the acidemia in hhs the arrangements of sodium secondary to the free water deficit and profound hyperglycemia are usually the most clinically relevant despite the complexity of its pathophysiology and the critically ill state in which many patients present the mortality of the eka in the united states is less than one percent in hhs mortality is in the ballpark of 10 percent in both cases if the patient does die the underlying trigger for the hyperglycemic crisis usually will have played the central role in the mechanism of death rather than the hyperglycemia crisis itself for example if someone who presents with dka secondary to sepsis or pancreatitis dies during the admission the cause of death is usually the sepsis or the pancreatitis rather than the metabolic derangements caused directly by the dka speaking of that what are the common triggers of dka it can be the initial presentation of type 1 diabetes or even type 2 diabetes in rare cases infections most often pneumonia gastroenteritis or urinary tract infection myocardial infarction pancreatitis medications most notably steroids but as mentioned sglt2 inhibitors are associated with eu glycemic dka there are other medication triggers as well intoxication with either cocaine or amphetamines physical trauma including burns and medication non-adherence which should be considered a diagnosis of exclusion meaning you should only attribute the dka to that if every other potential cause has been definitively ruled out i mentioned a minute ago that concurrent electrolyte arrangements are common in dka once again a hallmark feature is the elevated anion gap metabolic acidosis this is attributed to ketones but depending on the trigger there is the potential that a lactic acidosis could also be contributing i'm going to come back to why there are quotes around ketones in a few minutes derangements of potassium and phosphate are very very common though the potassium is the larger of those two concerns serum levels of either can be low high or normal but total body stores will always be low regardless of where the levels start or the serum levels start insulin treatment in dka will lower both serum potassium and phosphate due to transmembrane shifts hyponatremia is extremely common in dka as well most commonly this hyponatremia is true hypovolemic hyponatremia for example if the patient has been vomiting and unable to keep down solid food but has been able to take in water if the glucose is high enough it may be hyper osmolar hyponatremia in which the low serum sodium is only due to the hyperosmolarity from hyperglycemia this is what's seen with hhs there are two commonly cited correction factors used to adjust the sodium for the degree of hyperglycemia in other words to see what the sodium would be if the glucose was normal some clinicians adjust the sodium upwards by 1.6 ml equivalents per liter for each 100 milligrams per deciliter the glucose is above 100 so for example if a person's sodium was 130 and their glucose was 500 their sodium would be corrected to 130 plus 4 times 1.6 or roughly 136 unfortunately this correction is based only on first principles from many decades ago which involved significant assumptions about physiology and which has never been experimentally confirmed because of this other clinicians adjust the sodium upwards by 2.4 mil equipments per liter for each 100 milligrams per deciliter the glucose is above 100. clinicians who do this claim it's evidence-based however the actual evidence for this correction factor is a study in which six healthy volunteers had their blood glucose artificially driven up to 600 by the infusion of 20 dextrose it's a huge assumption that this correction factor would apply equally well in critically ill patients with diabetes so in short everyone knows sodium needs to be corrected in the setting of hyperosmolarity but no one truly knows how to do it in addition to these two forms of hyponatremia patients can also have pseudohyponatremia which is a lab artifact secondary to dka induced hyperlipidemia acute kidney injury is also common in dka which is usually secondary to dehydration and corrects rapidly with iv fluids i want to talk just for a minute about these specific so-called ketoacids produced during dka there are three that are clinically relevant the production of ketoacids starts with an excess of free fatty acids which undergo beta oxidation into acetyl coa acetyl coa that's not diverted into other pathways can be converted into acetoacetate some acetylacetate is irreversibly converted to acetone which is responsible for the fruity smell on the breath of some patients with dka while some acetoacetate is reversibly converted to beta-hydroxybutyrate if you have a background in organic chemistry from seeing the structures you can tell that acetoacetate is the only true keto acid here acetone is not an acid and beta-hydroxybutyrate lacks a ketone functional group so calling these ketoacids is two-thirds a misnomer and calling them ketone bodies is debatably preferable the standard ketone assay sometimes referred to as the nitroprusside assay or nitroprusside test which is the reaction that detects ketones onto your analysis or in the blood as a titration ratio only detects acetoacetate and acetone however beta-hydroxybutyrate is the predominant ketone body formed during dka luckily over the last two decades direct measurements of beta hydroxybutyrate have become more widely available and are resulted more quickly making this the preferred method of detecting ketone bodies in suspected dka in most u.s hospitals however this test is not as readily available as the nitroprusside test in all parts of the world at this point i'll move on to discussing the treatment of dka which has four primary components iv fluids insulin fixing electrolyte abnormalities and treating the underlying trigger the first three are almost always part of a hospital-wide dka protocol that has been devised and approved by an interdisciplinary team of endocrinologists critical care docs hospitalists nurses and pharmacists let's take a look at each component as a general rule you should avoid altering hospital dka protocols as they have been created specifically by people who honestly know and understand dka better than you do and who know and understand workflows in your specific hospital better however there are a few situations in which you may need to alter them which is why i'm going to go through what's typically included in the protocols these situations include times when the protocol isn't working or when the patient has another concurrent illness that makes the standard protocol potentially dangerous such as profound electrolyte abnormalities or advanced heart failure first regarding iv fluids vitals urine output and overall volume status should be monitored hourly the patient should typically be bolst one to two liters of isotonic fluid at the time of presentation there is a general sense that lactate at ringers is probably modestly better than normal saline if not for any other reason than because normal saline prolongs the acidemia if the serum sodium corrected for the degree of hyperglycemia is high after bolusing switched to hypotonic fluid for continued volume repletion but otherwise continue with isotonic fluid after the initial bolus typical fluid rates are in the 250 to 500 milliliters per hour range depending on the situation once the serum glucose is down below 200 to 250 milligrams per deciliter switch to a dextrose containing fluid like d5 half normal and further drop the rate down to the neighborhood of 150 to 250 as long as objective measures of volume status are also improving next regarding insulin glucose should also be monitored hourly the most common approach is to bolus either 10 units of iv insulin or 0.1 units per kilogram of iv insulin followed by a continuous infusion at 0.1 units per kilogram per hour insulin infusions are colloquially known as insulin drips however the need for the initial insulin bolus has recently been questioned in the literature but either way with or without a bolus once on the insulin drip the patient's insulin should be adjusted according to hospital protocol with a goal of decreasing the serum glucose by 50 to 75 milligrams per deciliter each hour for patients with mild dka that is dka with only modest volume depletion only modest electrolyte problems and normal mental status subcutaneous insulin right from the start can be considered instead of an insulin drip the main advantage of this approach is that it allows patients to be placed in lower levels of care within the hospital sparing icu beds a practice that anecdotally became more common during the coveit pandemic once dka is resolved overlap subq insulin with the insulin infusion for several hours remember that while a patient is on an insulin drip they need to remain npo as a sudden glucose load from a meal could cause substantial swings and insulin needs with electrolytes they should be checked every four hours until the dka is resolved or nearly resolved this is one on a very short list of specific circumstances in which potassium should be repleted to high normal levels if at any point the serum potassium dips below the normal range insulin should be held until the potassium is corrected once a patient with dka is receiving treatment hypokinemia is more likely a direct mechanism of death as compared to hyperglycemia there's been a lot said about phosphate repletion in dka but to summarize it you don't need to be nearly so aggressive with the foss as you do with the potassium so what are some signs that dka is resolved you'll see normalization of the anion gap the ph the patient's volume status and mental status and the beta hydroxybutyrate though this last one is not routinely followed serially what's not on this list glucose dka is usually resolved before the serum glucose is normalized and rapid normalization of glucose may not even be desirable as it could risk overshooting into hypoglycemia and a rapid decrease in serum osmolarity could theoretically cause cerebral edema coming back to the triggers evaluating and treating them as the final key component of dka management just going through some of the list for suggestions for every patient presenting with dka who does not have an easily identifiable trigger that includes a chest x-ray a ua and urine culture ecg plus or minus serial troponins depending on the age and presence of other risk factors lipase though because dka itself can increase serum lipase a mild to moderately increased lipase should be followed by a confirmatory ct scan of the abdomen and pelvis even if ct is not strictly necessary to diagnose pancreatitis in other situations most patients warrant a urine tox screen and last if you identify medication non-adherence as the trigger which has mentioned you should only do after excluding everything else on the list you still can't just leave it at that you also need to explore why the patient was not adherent is it lack of education lack of money lack of access to a primary care physician or to a pharmacy or just lack of motivation different problems will require different solutions i'll end by quickly running through some common pitfalls regarding pitfalls and dka evaluation there is a failure to sufficiently evaluate for a trigger a mistaken assumption that a modestly elevated lipase is indicative of pancreatitis a failure to identify the presence of euglycemic dka and a failure to identify total body potassium and phosphate depletion because the serum levels are initially normal last common pitfalls in dka management a failure to aggressively replete potassium to high normal levels a failure to hold insulin in the presence of hypokalemia focusing on glucose rather than focusing on intravascular volume acidosis and potassium a failure to overlap subcutaneous insulin and the insulin infusion for several hours a failure to realize that in unresolving acidosis despite improving glucose may be indicative of another process such as lactic acidosis and finally unnecessarily changing the hospital's dka protocol that concludes this video on dka if you found it to be helpful consider subscribing and checking out the rest of this intern crash course series [Music] you

Channel: Strong Medicine

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Length: 18min 16sec (1096 seconds)

Published: Tue Sep 14 2021