Diabetes Mellitus - CRASH! Medical Review Series

hey everyone so this is going to be part of three sets going over diabetes mellitus and this is going to focus on the pathophysiology of diabetes the medications use the oral and injectable medications that are used excluding insulin and some of the acute complications so that what is diabetes so diabetes affects 10% of all Americans and out of those nine out of ten suffer from type 2 diabetes so the terms type 1 and type 2 diabetes are the appropriate terms to use the there are old-fashioned terms that are used they're really not so much accurate so type 1 used to be called juvenile onset diabetes or insulin dependent diabetes and type 2 used to be called adult onset diabetes and non insulin-dependent diabetes and I'll tell you in a little bit why those are inaccurate terms so type 1 diabetes mellitus occur tends to occur in leaner patients it tends to occur in younger patients and it always requires insulin always always always and in the cause behind it is an autoimmune destruction of the beta cells in the pancreas which are the cells that release insulin they make and release insulin so if those cells are are destroyed then you're not going to have insulin release this tends to occur in children because I'll immune diseases can happen in children however it can also have an onset in adulthood so it's not necessarily juvenile onset but it does always require insulin now type 2 diabetes tends to occur in chronically overweight and obese patients and often can be controlled by appropriate diet and exercise but usually is going to require oral medication in addition to that diet and exercise type 2 diabetes may require insulin if the patient is not able to get their glycemic control in rain while they're on oral medications they may require your insulin and as a matter of fact as most type 2 diabetics progress in their illness their insulin resistance becomes so severe that they actually stop responding to insulin at all and as a matter of fact their beta cells can become so overwhelmed and so overworked that they can actually just stop secreting any appreciable amount of insulin so really type 2 diabetics can become insulin dependent so it's not appropriate to call type 2 diabetes in non insulin-dependent diabetes and also type 2 diabetes because of the obesity pandemic has been starting to occur in younger patients even children so to call it adult onset diabetes would also be not necessarily accurate diabetes is important to know about inside and out because it is a huge cause of morbidity in the US and particularly patients that you're going to see in the hospital they're sick patients they tend to be overweight they tend to be older and therefore they tend to have diabetes complications from diabetes there are a lot of them we're going to only talk about the emergent ones on this set of slides but I've devoted an entire set of slides to talk about the rest of them the emergent ones are diabetic ketoacidosis and hyperosmolar hyperglycemic state which used to be known as hyper katatak hyperosmolar coma we also have micro vascular complications which can lead to neuropathy macro vascular complications which can lead to nephropathy and then the neuropathic complications okay so how does diabetes present well regardless of whether it's type 1 or type 2 diabetes the symptoms tend to be pretty similar the history is where it's going to be different so the symptoms of diabetes is polyuria polydipsia and polyuria why because if you don't have insulin or you're not responding to insulin your cells are not getting any sugar and so as far as your body is concerned you're starving even though you've got all that sugar in your in your circulation your body thinks it's starving because it can't get the sugar in to the cells remember insulin is needed to transport glucose into the cells so some patients particularly type 1 diabetics because they're not overweight because they don't have any other symptoms because we don't we don't screen them for diabetes some type 1 diabetics will present with diabetic ketoacidosis and that's actually quite common because we're not screening children for diabetes now adults on the other hand if you have an overweight 48 year old man yeah you're going to screen him for diabetes you're probably going to have a passed glucose level on him and if it's elevated you might think okay we got to test you for diabetes before it gets to the point where he has a major complication now some type 2 diabetics will present with hyperosmolar hyperglycemic syndrome but the the nature of hyperosmolar hyperglycemic syndrome is that these patients are severely severely dehydrated and that doesn't happen usually in patients who can get out and about in our able body that usually happens more in sick and infirmed and older patients so it's very rare for type 2 diabetes to present with hyperosmolar hyperglycemic syndrome also diabetes can present with the overt microvascular and macrovascular or neuropathic symptoms of diabetes so diabetes may present with peripheral neuropathy it may present with gas droppeth ii so in that case then you'd have to take that into consideration so how do we diagnose diabetes if the patient has symptoms and this is rare but so let's say the patient has peripheral neuropathy or has symptoms of gas droppeth II and you get a random blood glucose and it happens to be over 200 if they have symptoms consistent with with diabetes as far as the complications of diabetes you can diagnose them just based on that random blood glucose this is generally not how patients are diagnosed with diabetes usually we diagnosed them earlier on so if the patient doesn't have symptoms which is usually the case when you're screening a 40 year old patient usually I think it's age 40 we start screening for diabetes if the patient doesn't have symptoms what we do is we when we screen the patient we have them fast and usually this is going to be when we're also screening their lipid levels because they have to fast for that too they fast overnight if their glucose levels are 126 or greater so this should be greater than or equal to 126 that is considered an abnormal glucose level and it's not enough though to just have that one abnormality they're going to have to come back and do the test over again having been fasted and have another abnormal result once you get to abnormal fasting blood glucose results that is diagnostic of diabetes now the oral glucose tolerance test is not so much used anymore for routinely diagnosing diabetes mellitus that's more for diagnosing gestational diabetes which I'll talk about in a different section so that's not for for diagnosing diabetes mellitus anymore now once you've diagnosed a patient with diabetes the next best step assuming that the patient is stable they're not the DKA patient or an HHS patient they don't have any other symptoms that need to be treated the next step in managing their diabetes is to get a hemoglobin a1c level because when we diagnose this patient with diabetes it's unlikely that they just develop the diabetes yesterday they probably had it for a while and so we want to see how bad it is and that will help us decide how to treat the patient so what is hemoglobin a1c it's a measurement of glycosylated hemoglobin and it's in a percentage so out of all your hemoglobin a certain percent of it is glycosylated and that percent is your hemoglobin one seat it provides the practitioner with an idea of how the diabetes has been controlled over the past three months and for a person who doesn't have diabetes so the normal level for a non diabetic patient is four point five to six percent now there's three ranges of a1c that's going to help us dictate therapy and these are based on the new a DEA guidelines and these just came out the past spring actually I believe it's the American College of clinical endocrinologists just came out with these new guidelines so you might not see these in some of your review books but these are new for 2013 so I would remember this and definitely remember it for for the clinic so there's three levels of a1c so you've got a new patient with diabetes to come in you get their a1c and you look at what their a1c level is there's three thresholds less than seven point five seven point five to nine or greater than nine point zero so formerly the best step in management was to start the new diabetic on a protocol of diet and exercise have them come back in another month and then check their a1c levels to see if it's improved or in three months while that's still recommended that they get diet and exercise at this point now we generally treat all type two diabetics with some kind of anti hyperglycemic medication so in addition to starting with diet and exercise we add metformin so remember I said those three levels seven point five seven point five to nine and greater than nine if the patient has less than seven point five percent a1c you can start them on mono therapy you could start them on diet exercise but like I said the American Academy of clinical endocrinologists they now recommend just starting right off with with mono therapy in addition to diet and exercise it's almost always that we use metformin that Mormon is much safer than the sulfonylureas and thiazolidinediones and it's much more effective so metformin is the drug of choice for mono therapy unless it's contraindicated and we don't use metformin in patients with renal disease or with liver or lung disease and that's because one of the adverse effects of metformin is acidemia so seven point five to nine point zero if they test in that range then we tend to start them out on dual therapy and we'll start them out on metformin of course something else that it's contraindicated and then add another medication if they're greater than nine point zero and the patient has diabetic complications so they have neuropathy they have they have a an increased creatinine they have let's say they've got gas drop a--they then we're going to start them on insulin therapy if the patient does not have symptoms then we're going to start them on a triple therapy so they'll still be on metformin and then two other medications if necessary metformin and then two other medications so as I mentioned medication is metformin is contraindicated in patients with renal failure liver disease or lung disease and that's because of the risk of lactic acidosis so what are the drugs that we use in diabetes the first drug that we're going to go to it's the cornerstone of therapy it has been and it still is despite the new recommendations it continues to be metformin so metformin is one of the most studied diabetic drugs and so we still go to it as the first drug now one of the exceptions to that is if the patient has renal liver or lung disease and the reason for that is because one of the dangerous side effects for metformin is lactic acidosis but unless the patient has renal liver or lung disease the first drug we're going to go to is metformin the sulfonylureas unfortunately are falling out of favor because of two side effects one it can cause hypoglycemia not appropriately dosed and to it is notoriously known for causing weight gain so that reduces patients compliance with their diabetic medication I wouldn't want to take a drug either if it made me gain 40 pounds in the first six months of therapy so so final ureas are generally falling out of favor but you can use a sulfonylurea as a first-line therapy if the patient cannot be on metformin for one reason or another that is all adding diodes include pioglitazone and rosiglitazone those have the this is also an older drug one of the nasty side effects from the thiazolidinediones is that it increases the plasma volume it can cause edema and so this is a problem if patients have congestive heart failure but it's I would say it's more patients comply with a thiazolidinediones better than metformin it also are better than sulfonylureas rather it also does not cause weight loss or weight gain so if a patient is on a sulfonylurea and they want to be on something if they're on dual therapy with metformin and they want to be on something that's not going to make them gain weight or then they can't afford one of the newer drugs then switching to a thiazolidinedione would be fine the only patients I would not prescribe it in our patients with congestive heart failure now the next - class of drugs and there's a couple other classes of drugs I didn't include here just for brevity but these two classes of drugs are very commonly used and these are newer the glp-1 agonists and the dpp-4 inhibitors and these are secreted cogs and the glp-1 agonists are newer and they're very very very well they're very good drugs let me put it that way because a lot of your patients with type 2 diabetes are going to be overweight or obese the glp-1 agonists have the singular positive effect out of all of the anti hyperglycemic of causing weight loss and so this will be a great drug to give to a patient who is overweight otherwise healthy has type 2 diabetes the only problem with it is that it's an injectable drug and so these patients have to take it subdermal ii now a lot of patients are very happily surprised by how easy and unobtrusive it is it's painless but that's something that you have to teach the patient it's also kind of expensive so that's another downside but this is a great drug for patient who are not happy in the sulfonylureas and thiazolidinediones and they've got insurance and it will cover glp-1 I guess what the glp-1 agonists do is they they are an agonist for a protein that increases the secretion of insulin so they're working at the beta cell they are a secreted GOG GOP one agonists are contraindicated in patients who have major medullary thyroid carcinoma or men type 2 syndrome which is multiple endocrine neoplasia type 2 syndrome it's also advised that patients stop glp-1 agonists if they develop symptoms of pancreatitis dpp-4 inhibitors include siddig lipton inlining clipton what the dpp-4 inhibitor is while dpp-4 is a protein that causes the breakdown of the glp-1 protein so by taking a dpp-4 inhibitor you're actually going to increase your accept of your endogenous concentration of glp-1 so they kind of do the same thing the difference is that dpp-4 inhibitors are weight neutral so they're not going to cause weight loss and dpp-4 inhibitors are also taken orally so that's another upside for patients that are needle phobic so this also is a drug that if the patient develops symptoms of pancreatitis it should be stopped and not restarted okay metformin is a is going into detail on that so along with diet and exercise this is a cornerstone of therapy and type 2 diabetics barring any contraindications this is the best initial pharmacologic management the adverse effects include lactic acidosis and GI upset okay so the so file ureas as I mentioned these are kind of falling out of favor and it's for two reasons one they're notoriously known to cause weight gain in diabetic patients and that's generally a problem because most patients who have diabetes are already struggling with their weight so to put on twenty or thirty pounds in a year while they're trying to trying to make positive changes in their life by getting their diabetes under control that's not really a fun thing for them so weight gain is a problem with sulfonylureas there's also an increased risk of hypoglycemia and along with insulin it is one of the most common diabetic drugs that can cause hypoglycemia so for those two reasons it is falling out of favor nevertheless it can still be an appropriate mono therapy particularly in patients where metformin is contraindicated the thiazolidinediones which include pioglitazone and rosiglitazone these are also sort of falling out of favor and that's because these can cause liver disturbances patients who are on T Z DS have to come in and get their liver panels checked approximately every three months and they cause water retention which can manifest as edema and so you want to try to avoid using thiazolidinediones in patients with congestive heart failure or our patients with copd they still again can be appropriate mono therapy in patients in whom metformin is contraindicated but the thing that thiazolidinediones have over sulfonylureas is that thiazolidinediones are weight neutral and so they will not cause that sort of weight gain that slip-on of urea is cause okay now let's get to some of the newer drugs the g-o-p one agonists so these are very attractive choices and then the reason that these are so attractive is because they the glp-1 agonists can cause weight loss and that is something that most diabetics need so it's effective in two ways and that it lowers your blood glucose and it also causes weight loss so the one problem with this is that it's taken by injection however the injection that the needle is really really really thin and a lot of patients are pleasantly surprised with how not obtrusive and painless this is so a lot of patients aren't going to have any problem doing this and and particularly when you talk to two patients who are overweight and you tell them that this can be associated with weight loss this is something that patients will want to do the problem with it is that it's expensive there are very few adverse effects with the glp-1 agonists however there are some contraindications patients with multiple endocrine neoplasia type 2 disease which is a genetic disease it's contraindicated in those patients because they're at risk of medullary thyroid cancer and in any patient with a history of medullary thyroid cancer glp-1 agonists are contraindicated they are associated with an increased risk of medullary thyroid cancer in patients who already have a genetic predisposition to developing that condition glp-1 agonists can be associated with acute pancreatitis there's no causal link between glp-1 agonists and pancreatitis but it is recommended that if the patient starts to develop the symptoms of acute pancreatitis that nine pain back pain they should stop taking their drug and see a doctor as soon as possible exenatide and liraglutide have been have been marketed as Byetta and Victoza and they still are under patent the dpp-4 inhibitors so dpp-4 inhibitors I want to start by talking about their mechanism so remember the GOP one agonist those work by increasing the secretion of insulin in the beta cells what dpp-4 is dpp-4 not a dpp-4 inhibitor but just dpp-4 itself is an enzyme and that enzyme breaks down glp-1 which has a very very short pathway like two hours and it breaks it down into inactive breakdown products so if you inhibit dpp-4 you're going to prolong the half-life of GOP one and therefore you're going to have an increased insulin secretion so that's a good thing if you want to reduce your blood sugar dpp-4 inhibitors are weight neutral and the thing that they have over the glp-1 agonists is that they're taken orally so a lot of patients would prefer that but they are weight neutral but that can be good if you have a real thin patient that you don't want to lose any weight dpp-4 inhibitors have very few adverse effects the one most prominent that happens is about one every three patients is nausea and vomiting but as long as you've warned the patient that those symptoms could come up they tend to be pretty compliant like the GOP one agonists they should not take these if they have a symptoms of acute pancreatitis and this is something that you should counsel the patient about before you put them on these drugs a dpp-4 inhibitor can be an attractive choice in a patient who is contraindicated for glp-1 agonist particularly because of the thyroid cancer contraindication a dpp-4 inhibitor can be an attractive choice okay so back to how we treat diabetes mellitus so remember that once a patient has established their diagnosis then we get an a1c level and the old way used to be to just start diabetes or start diet and exercise and see if they'd come back but the fact is that the American Academy of Clinical Endocrinology have said that that usually fails and so we should just go to start treating them medically as soon as they're diagnosed and so less than 7.5% they should be on mono therapy almost always that's metformin and unless it's contraindicated if they're between 7.5 and 9 we'll have them on dual therapy generally vally metformin plus another medication usually a a we would prefer to put them on the dpp-4 inhibitor or the glp-1 agonist but we can also use the safari urea or the thiazolidinedione if the patient's greater than 9 percent you have to ask yourself does the patient have complications do they have neuropathy do they have nephropathy do they have gastroparesis do they have visual loss in that case you should start insulin therapy if the patient does not have any complications then you're going to have them on triple therapy so metformin plus two of the other anti hyperglycemic s' okay so when do we treat patients with insulin so all patients with type 1 diabetes are treated within with insulin any patient who presents with an a1c level greater than 9 after they been diagnosed with diabetes and they have complications they should be treated with insulin and any patient that cannot control their a1c levels with maximal therapy they should be treated with insulin now the downside to insulin is that you've got inject it it requires a certain level of compliance because you have to have your insulin supplies with you you have to take it with you if you're going to a restaurant you have to make sure you have your insulin and you have to be aware of your diet and exercise muscle can absorb glucose and it doesn't need insulin to do that so if you go out and run three miles well that's great that you're getting exercise you've got to watch out because you may need less insulin and so it's always important to be taking your blood sugar before you inject your insulin because if your blood sugar is 93 as opposed to 193 you do not want to be giving yourself insulin if it's before a meal for instance okay certain insulin regiments now I've got dedicated an entire section to insulin regiments because they're so important and there are four different insulin regiments that are commonly used there's the once daily basal insulin regimen and that's usually used when a patient is also on some kind of anti hyperglycemic so you're just injecting a long-acting a long-acting insulin either in the morning or at night and that's just sort of supplementing your own phase up of your own basal insulin so you're giving yourself kind of a kick up for your insulin usually that'll be with insulin glargine or insulin rotameter there's the twice daily basal insulin regiments and this can be done without any kind of anti hyperglycemic therapy so you take a intermediate normal combination acting insulin in the morning and then in the evening and those are usually your 70/30 s or your 70 25 s and your 50/50 s there's a basal bolus or prandial regimen and that's where you take it's sort of a combination of a once-daily basal regimen where you're taking a long-acting insulin in the morning or in the evening and then before each meal you're going to supplement it with a quicker acting insulin and then there's a sliding scale regimen that tends to be used in hospitals and in siting scale regiments you take the patient's blood glucose every four to six hours and then you'll give them normal insulin based on that that's preferable in hospitals because a lot of patients and hospitals are on me different on different drugs they may have infections they may have inflammation which would cause a alteration and glucose levels and so it's useful to just respond directly to their glucose levels since they're in the hospital and there's professionals around who can monitor that okay so what are the emergent complications of diabetes so we talked about this a little bit earlier these are not these are these are emergent complications of diabetes so this isn't something that's supposed to happen this is something that goes terribly wrong if the patient's not being treated if a patient's treated they should not be getting these things so there's diabetic ketoacidosis this only occurs in type 1 diabetics and because type 1 diabetics can be children and we don't screen children for diabetes it can be a presenting sign of diabetes this could be the first manifestation of their diabetes and then there's hyperosmolar hyperglycemic State HHS this tends to occur on type 2 diabetics but it tends to occur because a patient is either non-compliant or they're older and infirmed and they can't drink water okay so diabetic ketoacidosis so what is this this is something that type 1 diabetics can present with and that's important to remember you may have a patient that presents with diabetic ketoacidosis that does not have a history of diabetes a lot of times this this well usually this is going to happen in children and that's because type 1 diabetes is generally juvenile onset but you can't rule it out just because you have an adult patient so what's happening here in DKA you have a severe insulin deficiency and it's severe enough to where the cells are going to shift to lipolysis now why is this well in your blood you have a ton of glucose so why do the cells need to shift to lipolysis if you don't have insulin then your cells as far as they're concerned they're starving because they're not getting glucose in and once they get to the point where they're starving enough they're going to shift their metabolism to breaking down fat and anytime you break down fat you create what are called ketone bodies now that's fine to a certain extent you could go on a low-carb diet and create ketone bodies but you don't do it to be suited to the extent that patients with DKA who have absolutely no glucose and their cells are doing it and when these ketone bodies spill out into the blood if they do it if there's enough of these ketone bodies it can actually precipitate it acidemia and that's because these ketone bodies are are they they're acidic and so what you can do is you'll note this when you check your your anion gap you will have an acid emia but you'll have a proton that's that's not contributing to your anion gap so you have your anion gap in sodium potassium subtracted from by bicarb and chloride and so the ketone body is not included in that and so the anion gap will be high because the ketone body is not included in that equation so a lot of times DKA is going to be precipitated by some kind of inflammatory process so it's not unusual for a foreign infection to spur on the DKA non compliance with insulin regimen and illicit drug use can also spur on DKA and that's really because in any kind of inflammation you're getting an increase in your metabolic rate so the cells are going to demand more energy and it's the same with illicit drug use particularly we see this with cocaine and methamphetamine the symptoms of DKA are similar to the symptoms of diabetes but they're going to be more pronounced so polyuria and polydipsia are always present nausea and vomiting malaise and fatigue and then you can get tachypnea and palpitations abdominal pain that's very present in DKA reduced appetite and at the end stages of DKA as the acidemia progresses altered level of consciousness actually progressing to Co MINDEF on physical exam you will see symptoms of hypovolemia so dry skin and mucous membranes reduce skin turgor patient could have could be hypotensive and tachycardic a lot of times you'll see confusion and the patient will often look very ill they'll have sunken eyes they may even be unconscious the diagnosis is going to be clinical and based on labs the most important labs that you can get are finger stick glucose and I would say I'm arranging this an order of importance so finger stick glucose would be the most important because you can rule out EK a if they got a normal glucose so finger stick glucose your analysis with dipstick the dipstick into the urine can tell you if you have ketone bodies and that's a pretty good confirmation of DKA along with an elevated glucose a CMP is going to be important to check your electrolytes and a CBC will be important to see if there's any type of infection going on arterial blood gases and cultures are good as well and you should also get an EKG on the patient because of some of the possible complications and serum levels of hydroxy butyrate can be useful for monitoring the patient's response to therapy so how are we going to make the diagnosis based on all these labs the glucose level will always be greater than 250 milligrams per deciliter often it's much higher I would say it tends to be around you know even more than five or 600 milligrams per deciliter so you're going to have a very high glucose your CBC is important because it could point you towards infection now I want you to remember that white blood cells are always going to be increased regardless of whether there's an underlying infection but if you have elevated neutrophils an increase left shift that suggests infection so you should culture the blood no matter what because infection can always be behind it but a left shift or elevated neutrophils is suggestive of an active infection going on which can spur on the DKA with your urine you're going to use a dipstick to check for glucose and ketones and that can be done right away if it's positive which it should be highly positive that's very suggestive of DKA your analysis will confirm this and you should also culture the urine your metabolic profile will show you hyperkalemia and hyponatremia and a low bicarb why the hyperkalemia because potassium and glucose travel together so if you have low insulin you're not getting glucose into your cells and so your the glucose is remaining in in the blood that's why we get high glucose and the potassium is going to remain in the blood and that's causing the hyperkalemia you'll have a hyponatremia as well and a low bicarb this will result in a high anion gap and that's suggesting both the presence of the ketone bodies and the fact that you have metabolic acidosis your arterial blood gases will confirm metabolic acidosis like I said the hydroxy butyrate will be high and this is a great way to to have a laboratory indicator of how the patient's responding to therapy so the treatment the treatment is going to be primarily based on your ABCs so what are your ABCs it's going to be it's going to be air space breathing and circulation so the circulation here is at risk because these patients are at depleted fluid volume and so you're going to want to replenish their fluid as quickly as you can you'll want to start in normal saline bolus immediately as soon as you see a patient that looks volume depleted you're going to want to give a normal saline bolus and you should actually give up to 3 liters of normal saline in the first hour so as at least one but as many as 3 liters of normal saline in the first hour so you're going to be using white board scre another leader should be given in the second hour and then another liter can be given over the subsequent four so you're going to be giving up to five liters of normal saline so that's quite a bit but these patients tend to be very volume depleted and you've got to get that normal saline in as quickly as you can once you start administering the normal saline then you can go ahead and administer insulin and you're going to use normal insulin here normal insulin is a short-acting insulin it doesn't work as quickly as list pro or ass part but it works much quickly than NP NK h or Dead Amir or glargine so you're using normal insulin for DKA and it works relatively quickly and you're going to dose at at zero point one units per kilogram per hour you should be getting a CMP you should have a CMP beforehand and you should be getting your electrolytes frequently afterwards probably at least every hour because you're going to suggest you're going to expect that this patient is going to go into a hypokalemia now why is that well they're starting out hyperkalemic but even though the patient is hyperkalemic they're only hyperkalemic because they're fluid deprived and because the potassium is unable to enter the cell once you start insulin you're expecting well when you start insulin and your normal saline bolus you're expecting one the the blood is going to become more dilute as your volume status improves and when insulin is administered potassium is going to move out of the blood and into the into the cells so you're going to expect a pretty quick drop in that potassium level so you will go from hyperkalemia and eventually you probably will go into a hypokalemia so the rule is and you're almost always going to be giving potassium to these patients as you look at their potassium levels as they come back if their potassium levels are more than six you're not going to be administering any potassium at all once it goes below six four point five to six you'll start them on ten milli equivalents of potassium chloride if it's between three and four point five you should administer 20 milliequivalents of potassium chloride and if it's below three then you should stop the insulin and this is another reason why EKG is important because remember the fact that potassium can have on the heart whether it's high or low now the normal levels for potassium is three to five point five but notice that we're going to actually start administering potassium chloride at potassium level of six and that's because again we're expecting the patient to go into hypokalemia and by hypokalemia I mean we expect them to be at risk of hypokalemia so we're treating it prophylactically I should say Oh along with treating the diabetic ketoacidosis of course we should be treating the underlying cause if the patient has symptoms of pneumonia we should be getting a chest x-ray if they've got a symptoms of UTI meaning they've got elevated nitrites and red blood cells and white blood cells in their urine we should be giving them antibiotic for that but treating the underlying cause is always going to be important and then something that the USMLE likes to throw at you is do you want to treat the patient with bicarbonate and let's say the patient has an acid emia and they're 7.15 no you're not going to treat them with bicarbonate you're going to treat the underlying cause and that should treat the acidosis now at times you will give bicarbonate but I would say on the USMLE it's almost always the wrong answer bicarbonate is usually given when the patient is comatose and their their acidosis is extremely severe and by extremely severe I mean less than 7.05 less than seven but on the USMLE bicarbonate is going to be generally the wrong answer you're going to want to give fluid replacement administered insulin keep an eye out on those electrolytes and replace potassium as needed after the emergent treatment of course like I mentioned the underlying cause should be found all patients should be admitted to the general Ward's or to the ICU and put on a sliding scale and that's why we search for a cause of the DKA the patient can be discharged once the patient is well enough we know that they're going to comply with the daily insulin regimen and the underlying causes result so if they still have pneumonia if they still have a UTI we're not letting them out yet we want to fully resolve the underlying cause and we must emphasize the importance of adhering to a strict insulin regimen ok hyperosmolar hyperglycemic state so this is formally known as hyperosmolar nonketotic coma or honk h o NK or H ONC and this is this is different from d ka so the reason that we change the name is because patients can actually with hyperosmolar non-ketotic coma they can be positive for ketones so you don't want to have the misinterpretation that just because the patient has positive ketones that they're diabetic ketoacidosis because they might not be necessarily so they may be positive for ketones but it's not going to be as positive and they're not going to be Kido acid otic and also we change the name because not all patients are in a quote/unquote coma there is almost always a decreased level of awareness confusion but they're not always going to be in a coma so the cause for hyperosmolar hyperglycemic state is the most common precipitating factors is one non-compliance with insulin regimen but usually it's going to be due to chronic dehydration what happens in a patient who is chronically dehydrated as they become more well as they become if they don't let's say they don't take their insulin their glucose level goes up as their glucose level goes up they spill more glucose in to the nephron and out through the urine when there's more when there's more glucose in the tubules that's going to draw fluid out as you draw more fluid out you become more hyperosmolar your ear you become more dehydrated and the more dehydrated you become the higher your relative level of is because your glucose level is going to be more constant it's going to be higher when your blood is more concentrated so dehydration Fito well high glucose levels feed into the dehydration because it calls causes polyuria and the polyuria feeds back into the high glucose level because it concentrates the blood and so it's this vicious cycle going on the symptoms are going to be acute loss of consciousness decrease level of awareness focal or global neurologic deficits usually either global neurologic deficits sometimes you may see seizures but a lot of times you're going to know that these patients have type-2 diabetes thirst can also be a symptom and it usually is a symptom but if the patient is is not aware they might not they might not relate that to you and then Polly area but if the patient is critically dehydrated they may not have any urine so look for a focal and global neurologic deficits acute loss of consciousness in a patient with known type 2 diabetes diagnosis again is going to be clinical and laboratory the most important labs here are going to be your finger stick glucose your CMP your urinalysis Plus dipstick and your CDC your finger stick glucose is going to help you diagnose HHS because patients with a with HHS are usually going to have glucose levels that are so high they're going to be almost always above 600 and even higher sometimes your CMP is important to help you find out your plasma osmolarity and the UAE and dipstick is helpful sort of to differentiate this out from DKA if you need to and then a CBC is useful as well because there are neurologic symptoms you're going to also want to get a CSF just to exclude any kind of trauma or any kind of and then chest x-ray is useful it's easy you can look for infection there pneumonia is a very common cause of infection particularly in elderly people where this usually strikes an EKG is good to get and then a CT of the head so for diagnosis the glucose level is going to be above 600 milligrams per deciliter but often it's much higher CVC just like in DKA the white blood cell is going to be increased regardless of whether this is an infection or not but the left shift is going to suggest an infection and you should culture the blood your analysis that you get a dipstick it should be highly positive for glucose but not so much for ketones your analysis will confirm this and you should culture the urine as far as your CMP the electrolytes are going to be are going to vary they're not going to be as cut-and-dry as the as DKA but what you will see in hyperosmolar hyperglycemic state is a high serum osmolality and that's because you're peeing a ton and so your your blood is is just getting more and more concentrated so often it's going to be greater than or equal to 320 and that's really high you're also going to see because of the dehydration you're going to see a zty neon what's a zty mia is just an elevated vun and so an elevated vun with a pre renal picture will be seen pre renal sot mia comes from dehydration and so because we have less perfusion to the kidneys the kidneys respond and the creatinine level goes up but the UN level goes up even more and so the B UN creatinine ratio will be greater than twenty to one and that is a pre renal azo tinea picture and it can't remember that go back and look at the pre renal is a Tamiya section that I did in the nephrology section so AZT Mia with a pre reno picture really points us towards hyperosmolar hyperglycemic state okay the treatment for HHS the primary goal is going to be to replenish fluid volume so why do we want to replenish fluid volume first insulin replacement is secondary because in these patients the primary problem is that they are dehydrated and this can be deadly so the primary goal first is to replenish the fluid volume plus because we don't know their oh if they're hyper Colima core hypokalemic or normal k lemic if we give potassium or sorry if we give insulin they may go into very deadly hypokalemia so we want to get their their fluid volume replenished first so in unresponsive patients the very very very very first step of course following your ABCs it's going to be to secure the airway now after you've done that or if the patient is responsive and breathing you should give 1 to 2 liters of normal saline over the first hour and then the rule of thumb is generally to replace half of the estimated fluid loss in the first 12 hours and the other half in the next 12 hours meanwhile you should be getting cereal CMPs why because you want to look at the electrolytes and you want to look at how the kidneys are doing once the A's ot mia has results so once you're between 10 to 20 to 1 so a b1 creatinine ratio between 10 and 20 to 1 then you've resolved the pre renal AZT mia at that point then you can start insulin so once the a is a teeny is resolved and a normal bu and creatinine ratio is established you can start insulin just like in DKA you're going to want to monitor your potassium while you're giving insulin because insulin causes the blood potassium to drop and so the insulin therapy just like in DKA is regular insulin it's zero point one units per kilogram per hour and we're going to target a glucose between 200 and 300 milligrams per deciliter at that point then the patient can be brought back on to their oral therapy so remember that the potassium will drop once the potassium hits five milli equivalents per liter which it will and oftentimes it will before you get back down to 300 you'll want to start potassium chloride 10 milli equivalents per liter in their IV at once it hits 5 milli equivalents as far as how we their disposition once the patient is stabilized and they're in the 200 to 300 glucose range and an underlying cause is being investigated you should transfer them to the ICU or to the general Ward's generally if they need to seek your airway you're going to be transferring out them to the ICU otherwise the general wards or an intermediate ward would be fine neurological sequelae will often last for weeks even once the glucose and and everything else has been corrected so a lot of times they're going to need to be in the hospital for a while and you can step them down to the wards from intermediate or to intermediate from the ICU but usually they're going to need to be in the hospital once the patient is discharged what you once the patient's neurologic symptoms have improved then you can discharge the patient as long as they're able to sufficiently care able to care for themselves and for their oral medication and insulin regimen and their own glucose monitoring you should consult an ad a diabetes educator if one is present or give education yourself as far as making sure that they're taking their diabetes drugs or their insulin and you should also consult social services particularly if the patient lives alone if they live in a nursing home because generally patients should not get like this this comes from yes both not taking your insulin but can also come from severe dehydration so if the patient's in a nursing home we're wondering what's going on and this can be associated with elder abuse so social services can be an appropriate consult in this case and then home care can be useful if the patient lives alone just to help them do appropriate measures at home to keep this from happening again and for information on new chronic complications including neuropathy nephropathy and gastroparesis see the lecture on outpatient management of diabetes mellitus

Channel: Paul Bolin, M.D.

Views: 143,340

Rating: 4.8350515 out of 5

Keywords: Medicine (Field Of Study), United States Medical Licensing Examination, Internal Medicine (Medical Specialty), Endocrinology (Medical Specialty), Health Care (Industry), Health Care Provider (Profession), Pharmaceutical Drug (Medical Treatment), Pharmaceutical Industry (Industry), Diabetes Mellitus (Disease Or Medical Condition), new drugs, physicians, health insurance, medical education, disease, biomedical, malpractice attorney

Id: fZmKrFGokfs

Length: 53min 8sec (3188 seconds)

Published: Sat Nov 21 2015