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Approach to Hyperglycemic Emergencies

Feb 21 | 2:30 PM

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two metabolic disorders characterised by insulin insufficiency and severe hyperglycemia, with mortality rates ranging from 2.5 to 10%. These situations require urgent medical care since they can result in catastrophic complications such as coma and perhaps even death if not corrected. Dr. Pratibha Dileep will discuss a DKA and HHS management approach based on current evidence, as well as a simplified emergency department management pathway.

[Music] good evening everyone good evening to the faculty all our doctors yes so today i welcome you for this session on approach to management of hyperglycemic emergencies i'm dr brushali from netflix and i would like to welcome you all today we have with us dr pratibha dilip she is a renowned critical care specialist in ahmedabad who is currently practicing insiders hospital she has more than a decade of experience working as a critical care doctor and has gained proficient skills and knowledge in the segments so without further delay ma'am i would hand it over to you now thank you thank you vishali yes ma'am so good evening friends today i'll be talking about hyperglycemic emergencies as all of you are aware that hyperglycemia or rather diabetes is quite a quite a common uh phenomenon in today's modern i see almost 50 percent of our patients are having diabetes and incidence of diabetes is on the rise world over approximately one in two thousand iddm patients develop a decay almost two episodes per 100 patient years and about three percent idiom initially present as decay exact incidence of hyperosmolar hyperglycemic syndrome is not well known but it is also seen in modern icu it is associated with very high mortality almost as high as 20 percent mortality so it's important that we know about it though the incidence is not very high but whenever it does come it is associated with quite high mortality and usually it is precipitated by concurrent severe illnesses so whenever a diabetic presence with whenever a diabetic results with any other severe illness this is the possibility one has to keep in mind as all of us know that diabetes can be iddm or nidtm iddm is the result of interaction between genetic environmental and immunological factors leading to destruction of beta cells of the pancreas and insulin deficiency the key factor point is insulin deficiency and usually it is the autoimmune process which triggers iddm either it could be started by an infection in childhood or some environmental factor while insulin resistance is the key factor in niddim so the level of insulin is high in the body in nidtm unlike iddm worthy there is absolute insulin deficiency excessive hepatic glucose production abnormal fat metabolism low grade systemic inflammation and visceral obesity characterize niddian these are the important uh parameters to determine nibb now what are the type of hyperglycemic emergencies we see uh in today's lecture i will be talking mainly about diabetic ketoacidosis and hyper osmotic hyperglycemic syndromes in nidtm which was earlier also known as hyperglycemic non-ketotic coma hocm but not anymore it is now known as hyperglycemic hyper osmotic syndromes uh decay diabetic ketoacidosis the commonest symptom is nausea vomiting polyuria abdominal pain shortness of breath and usual precipitating events are the patient has skipped the insulin dose as you all know that the iddm usually presents in young children so they sometimes skip the insulin dose there is an occult infection which can precipitate or some tissue ischemia say pancreatitis or any other organ ischemia can produce this in young young children drug abuse like cocaine sometimes pregnancy these are the precipitating events for decay and sometimes almost three to four percent of iddm patients they present with dk physical findings are usually tachycardia these patients are severely dehydrated usually hypotensive the most important physical examination finding is acidotic respiration also known as kosumal spreading they have usually abdominal tenderness they are very lethargic and sometimes can be obtained also now it is a person it is a life threatening emergency of iddm usually precipitated by infection it occurs because of dysregulated catabolic state of insulin deficiency coupled with high level of counter regulatory hormones this is the key factor along with deficiency of insulin there is high level of counter regulatory hormones counter regulatory hormones meaning thereby glucagon corticosteroids the levels are much much high impaired glucose utilization increased glucose production and increased glycogenolysis all the three contribute to hyperglycemia because of lack of insulin the glucose is not utilized and hence the liver produces more and more glucose and the glycogenolysis all the three contribute to severe hyperglycemia now increased glucose levels lead to hyper osmolarity and osmotic diuresis most of these patients have complaint of polyuria hence polydipsia and lack of insulin promotes fat catabolism and hence there is ketonemia because ketones do not require insulin for their consumption for their utilization hence these patients have ketonemia which is a which is the most important difference between diabetic ketoacidosis and hyperosmotic hyper glycemic syndromes where there is because there is insulin is present ketonemia is not usually seen now normally free fatty acids are converted to very low density lipoproteins in liver but high glucagon alerts this mechanism alters this mechanism leading to ketone body formation and hence these patients have high ketone levels and they become acidotic ketones though these patients have good capacity to excrete the ketones because most of these patients are young patients and they have normal renal functions so the body's buffering capacity can get rid of these ketones but once the capacity is exhausted these patients develop acidosis so the diagnostic criteria for dka is blood glucose more than 250 milligram per deciliter ketone ketonuria metabolic acidosis bicarbonate less than 18 milligram per liter breathing these are the important drag diagnostic criteria all of them are a must coming to hyperglycemic hyper osmolar syndromes that is also known as hhs this is exclusively seen in niddm patients more than 90 to 95 percent patients are ni ddm rarely we see in iddm also especially in the older age group and it is more commonly seen in obese patients this may be true because most of the time obesity is associated with niddim so this may not be an exclusive factor but since obesity is associated with niddim we are seeing an association of hhs with an iddm now if not treated on time can have very high mortality almost as high as more than 20 percent probably the high mortality is because of concurrent many illnesses which precipitate this event rather than per se hhs now this was also known as hyper osmolar non-ketotic coma h-o-n-k now this terminology has been discontinued because many of these patients are not comatose out of 100 patients of hyper osmotic hyperglycemic syndrome only 10 to 15 patients are comatose so this [Music] terminology is not used any longer now this is a just a spectrum of from hyperosmotic state to hyperosmotic coma most common precipitating event is usually infection severe insult of other systems like myocardial infarction or cerebral vascular accidents or even trauma can precipitate hhs in niddm patients and majority of these patients are seen in fifth or sixth decade so whenever an elderly patient or six decade or fifth decade person with niddm comes with very high glucose levels chances are that this person is likely to have hhs rather than dka now hallmark is hyperglycemia induced severe volume depletion without acidosis volume depletion is seen even with decay but it is usually associated with severe metabolic acidosis which is which is classically absent in hhs mortality is much higher relative insulin deficiency and inadequate fluid intake are the precipitating causes patients usually die of dehydration and concomitant medical conditions average water deficit can be as high as 8 to 10 liters in these patients uh the problem is that this high deficit because these patients are usually older age it is difficult to replace these this much volume without causing cardiac compromise and sometimes the morbidity occurs because of that the diagnostic criteria is severe hyperglycemia uh six hundred two thousand milligram per deciliter sometimes it is not measurable by the uh glucometers with high hyper osmolarity more than three hundred and twenty million small per kg per liter profound volume depletion altered mental status altered mental status is seen in almost 60 to 70 percent of patients with hyperosmotic hyperglycemic states rather than in comparison to dk where it is seen only in eight to ten percent patients now pathophysiology of decay if we see compare the two decay has circulating insulin is low or absent while circulating insulin in hhs is high increased lipolysis due to lack of insulin as we discussed earlier while there will be hardly no minimal or no lipolysis rarely we can have ketones even in hhs also but usually they don't cause acidosis if we see acidosis in a hyper osmotic hyperglycemic coma usually it is because of concurrent renal impairment so it is more of because of renal failure rather than because of ketosis you have high level of glucagon while the glucagon level is low in hhs high ketoneemia leads to metabolic acidosis no or very minimal acidosis in hhs not very high osmolarity but more than 300 while here the austenite can range from 320 to 420 also and they have much greater free water and electrolyte deficit lab parameters in dk and hhs in dk the glucose can be variable while hhs it is usually more than 600 to 1200 osmolality as i said usually could be normal or mildly raised but not usually more than three hundred and ten while hhs it is more than three twenty sometimes can go up to four hundred also sodium is usually normal or low pseudohyponatremia because of high glucose level the corrected sodium should be calculated in these patients it is usually calculated by for every increase in glucose by 100 milligram the sodium drops by 1.6 milligrams so when a patient comes with normal sodium usually these patients are quite dehydrated the actual sodium may be much much higher than that anion gap the decay always leads to high in iron gap metabolic acidosis it is always more than 12 million while an and gap in hhs could be normal or maybe low because of concurrent renal failure phosphorus is usually low in decay while it may be high or normal in hhs because of associated severe rhabdomyolysis ketones usually very high in decay as by definition they are usually high they may be normal or they may be mildly raised in hhs abg ph can range from 6.8 to 7.2 while usually it is above 7.3 in hhs so these are the diagnostic differences between these two conditions now how do we manage these patients the basic parameters of treating both the conditions are same the most important thing is fluid replacement so let's first talk about decay the fluid replacement most all the dka patients all of them are severely dehydrated because of severe osmotic diuresis as we discussed earlier and associated vomiting along with poor intake so aggressive fluid resuscitation almost 15 to 20 ml per kg bolus of normal saline followed by 200 to 250 ml per hour is usually required and usually these patients are quite young patients have normal cardiac functions and normal renal functions so they tolerate large amount of volumes sometimes they may require almost 2 to 2.5 liters of bolus over 1 to 2 hours and then the subsequent volume replacement could be in the range of 200 to 250 ml per hour now choice of fluid uh is a tricky thing uh initial choice of replacement should always be with normal saline irrespective of the sodium levels but one must keep checking the sodium levels corrected sodium should always be checked if corrected sodium is normal then that means the person is quite dehydrated in such a scenario one may choose to use 0.45 line or finger select it but the initial bolus should always be normal cell line resolution of dk is associated by measuring beta hydroxybutyrate or by measuring an iron gap so these patients should be frequently tested for the electrolytes as well as beta-hydroxybutyrate how do we manage these patients the general principles volume depletion and hyperglycemia are the main concern of diabetic ketosidosis and hyperosmotic hyperglycemic states careful monitoring of hydration electrolytes and sugar are crucial underlying precipitating cause must be dealt with aggressively like exam for example infection anywhere infection any other stressful situation like pancreatitis or any trauma or any cardiac condition should always always be looked into occult infection should be treated in these patients some people prefer to give a prophylactic antibiotic also broad spectrum antibiotic in patients those who are very sick frequent lab monitoring of capillary blood glucose electrolytes and acid based status must be done initially as frequently as every two hours sometimes every hourly also may be required but by and large first 24 hours are very crucial if in that phase the patient has been manageable then the monitoring has to be less frequent two to two point five liters of point normal cell point nine saline in first one to three hours followed by 200 to 250 ml per hour of 0.45 saline or rl must be infused till sugars are below 250 milligram per deciliter now beta hydroxybutyrate is synthesized three times greater than acetoacetate so if urine ketones are checked one may have less reliable uh answer because urine ketones may still remain positive or negative one must check one must monitor serum ketones instead of urine ketones electrolytes in decay are very crucial sodium potassium and phosphate need special attention as i said sodium may be falsely low in presence of severe hyperglycemia so if the person has normal saline and normal sodium that means this person is actually having hyper naturemia so extra cellular potassium can be very high because of lack of insulin which may decrease once the insulin is administered so all these patients when they have uh decay their total body potassium is usually low even if the extra in even if your serum potassium is high so extra cellular potassium may not really reflect the total potassium levels phosphate level is initially high but with administration of insulin it may go low serum phosphate as low as point less than one is associated with serious arrhythmias these patients can develop serious arrhythmias because of low potassium low phosphate so it is important that we keep checking them frequently sometimes potassium phosphate replacement is a better choice than potassium chloride potassium phosphate was earlier not available nowadays it is available if frequent monitoring is possible then potassium phosphate also is a good choice for replacement of potassium in these patients microbe supplement must be avoided unless the ph is less than 6.9 there is a controversy in this some people say below 7.1 backup supplement should be considered but by and large bicarb supplement is detrimental in treatment of diabetic ketoacidosis potassium supplement diabetic ketosidosis are usually always potassium deficient even if the initial potassium is high so replace potassium almost 10 milligram per hour when potassium is between 5 to 5.2 per liter this is a contrary to our common practice 5 to 5.2 normally we don't give potassium in other conditions but as i said that these patients are intrinsically potassium deficient so once we start insulin the potassium is going to go inside the cells and the patient can develop severe hypokalemia so it is better to start with small dose of potassium supplement in these patients even if the potassium is between 5 to 5.2 ecg and creatinine if they are normal then you must start with potassium supplement when the potassium is less than 3.5 the replacement can be required maybe is 40 to 80 milligram per hour in fact it is suggested that insulin should not be started unless the potassium is more than 3.2 so only if the potassium is more than 5.2 do not supplement potassium monitoring of potassium must be done frequently as frequently as four early or six hourly till the patient is stabilized now coming to sodium corrected sodium is always higher as i said then measured add 1.6 milligrams of sodium for every 100 milligram milligram high in sugar say the sugar is 600 milligram then you have to add 6 into 1.6 into the measured sodium and measured sodium say if it is 130 so then you have to add 9.4 into that now patients with dk and normal saline i mean decay and normal sodium is usually hypernatremic hence their volume depleted after initial correction with normals aligned the fluid should be switched to either 0.45 line or normal or being reselected to avoid severe hypernatremia now how do we go about insulin now insulin is the main stay of treatment it must be started only after adequate volume resistation has been done normally when dka patient comes the first thing is to start insulin but the important point here is that volume resuscitation and potential correction should take precedence over starting with insulin the simultaneously a bolus volume should be given and potassium should be checked and potassium should be corrected after that only the insulin should be started otherwise the patient can develop severe hyper hypokalemia and can have refractory arrhythmias now rbs must be checked hourly and it should fall 50 to 80 milligram per deciliter per hour not faster than that because faster than that correction can cause severe osmotic derangements and altered sensorium in these patients as far as the insulin regimens are considered concerned there are various regimens which people use the standard regimen is start insulin with 0.1 unit per kg bolus say a 60 kg per patient is there then six units bonus followed by six units per hour by iv infusion and keep checking the insulin i mean sugars if the sugars they start dropping faster than 50 to 80 milligram per deciliter then half the rate of insulin till the sugar levels are 250 this is the standard method but people use different methods to determine how to use insulin and individual comfort level is also important the initial bolus remains the same 0.1 unit per kg per hour followed by people use if the sugars are more than 400 then they as long as the sugars are more than 400 they continue with 5 ml per hour and then as the sugars start dropping the insulin levels are reduced individual comfort is more important than that ketonemia may persist longer than hyperglycemia this is an important point these patients can remain ketotic even if they have become maybe less hyperglycemic and abrupt withdrawal of insulin can worsen ketoacidosis so it is important that once the patient has become the sugars have come down to less than 250 the volume the fluid should change to dextrose normal saline rather than normal saline dextrose normal saline with 10 to 15 units of insulin in the saline would take care of this keto anemia so that is one important point one must remember while treating decay how do we determine resolution of decay the clinical examination is the key patient's breathing settles down the patient looks well hydrated ketoacidosis results once insulin is administered insulin reduces lipolysis hence ketone formation is reduced and the ketones are used peripherally because of the presence of insulin it suppresses the hepatic ketone body formation so the level of ketones start going down and it promotes bicarb generation so that is how administering exogenous bicarb can be detrimental to these patients by as soon as the decay starts resolving the bicarb levels start improving if you do a blood gas and you see that serial blood gas shows improving trend of my cub that means the ketosis has started to dissolve now coming to hyperosmotic hyper glycemic states the treatment is the baseline remains same maintaining abc airway breathing and control circulation aggressive hydration with isotonic fluids potassium supplement and insulin infusion again here the hydration takes precedence over insulin and potassium supplementation again takes precedence over insulin infusion the basic principle remains just the same now usually these patients are more volume depleted than dk one to three liter of normal saline in one to three hours followed by 0.45 ns may be more suitable the only difference here is that patients are much older and many of them have concurrent cardiac problems many of them would some of them have a myocardial infarction so one has to take care that they don't precipitate pulmonary edema in such patients cardiac status should be checked diligently calculated fluid deficit should not be corrected within few hours it should be corrected over one to two hour days to avoid osmotic demyelination many of these patients develop neurological deterioration because of over zealous fluid correction when one must try to correct the deficit over 48 hours dehydration must proceed insulin as i said earlier volume resuscitation addresses hyperglycemia hyper osmolarity and dehydration insulin dose remains just the same 0.1 unit per kg bolus followed by 0.1 unit per kg per hour serum glucose must be maintained around 250 to 300 milligram per deciliter until the plasma osmolality comes down to around 315 either very rapid drop in plasma hospitality can cause cerebral edema and convulsions in these patients these patients are usually potassium depleted despite initial hypercalcemia hyperkalemia just similar to decay so potassium supplement must begin once the potassium is less than three point three to four milligram the only difference is that many of them have associated rhabdomyolysis so you can have uh severe hyperkalemia if you start potassium supplement at higher than fourth milligram furniture unlike decay where rhabdomyolysis is not very common phosphate calcium and magnesium must also be checked renal failure patients can have falsely high magnesium levels also otherwise magnesium supplement may be required in these patients the complications of hhs as i said that it is associated with very high mortality it is a pro thrombotic state and it promotes rhabdomyolysis so these patients many a times have associated renal failure they can have strokes because of prothambatic state cerebral or pulmonary edema is very common if it is not treated properly dyselectrolytemia again very common in these patients and most of these patients as i said are elderly they can have associated cardiac complications because of aggressive volume resistation so to summarize decay and hyperosmotic hyperglycemic syndromes are relatively uncommon medical emergencies i was checking in my own icu almost 45 to 50 percent patients are diabetic in icu but you see dk almost say once or once or twice at the max in a month while hyperosmotic uh hyperosmotic hyperosmo uh hypoglycemic states is seen as low as once in three to four months but whenever they do come a diligence in the management is a must because these are quite rewarding if we if treated in time properly hhs is associated with very high mortality hence concomitant factors should be managed well treatment of precipitating events is as crucial as the primary treatment so this is the important point one must remember this lecture has been the references are as shown here on the screen besides these conditions we see quite a few especially post covered quite a few patients coming with severe hyperglycemia though they do not fit into the definition of hyper or smaller states but many of these patients are on steroids many of these patients have other conditions so we saw quite a few patients coming with severe hyperglycemia requiring insulin infusion that they may not fall into the category of diabetic emergencies but the management remains more or less the same thank you very much now i can take questions yes ma'am and thank you so much for that very nice session the way you explain the diagnosis the treatment how it varies in education decay and how the treatment also would keep on wearing as the fluid levels and the volume depletion or volume increased so that was really very informative i think one question has come is it reasonable to give prophylactic antibiotics yes ma'am i would say say in principle there is unless we find some infection no need to give antibiotics but many times when the patient is very sick it is very difficult to rule out infection so a small antibiotic broad spectrum antibiotic very high antibiotic is not needed but small antibiotic like ceftriaxone can be considered in these patients when they are very sick stop it after 48 hours if you don't find any infection maybe because at the time of admission sometimes the infection is not picked up after 48 hours you can always stop it outline protocol i am not really aware of that dr josephine is asking when do we start subcutaneous insulin say subcutaneous insulin should not be given in the initial state when the patient is so dehydrated and hypovolemic it should always be given only after in dk only after the ketosis has settled in hyperglycemic states also when the patient is well hydrated because subcutaneous insulin will not get absorbed unless the patient is properly well hydrated hemodynamically stable it should not be started uh dr eunice is asking most patients present with very high sugar 500 and more yes they don't fall in the either category neither dk nor hhs and they usually don't have symptoms so what could be the cause and the treatment that's what i said that we are talking about the diabetic emergencies but in actual we see quite a few patients as i said the incidence of diabetic ketoacidosis and hhs is quite small but incidence of severe hyperglycemia is quite common especially we saw it in the covid pandemic many patients presented with 500 milligram per deciliter sugar they were not falling into category of hhs i personally feel that first time detected or any patient having more than 400 milligram per deciliter of sugar we start with insulin infusion only in our unit so that we come to know what is the requirement of insulin by titrating and hence we can whenever we put them on intermittent insulin we have some guideline how to go about it all right dr ritwik is asking how do we transition from iv insulin to subcutaneous enzyme so as i said the iv2 in iv2 subcutaneous should always be done only when the patient is uh you know well hydrated as the oral feeds have started because the subcutaneous insulin will be a bolus insulin it will be you know if the patient's uh hemodynamics are not good it won't get absorbed and it should be preprandial so it should always be started once the patient starts eating orally ketosis has been corrected and hydration is well maintained okay is there any protocol that how often should the electrolyte and the abg investigations be done see books mentioned as as much as two hourly three hourly but practically speaking it is it is very expensive and it is not really feasible to do so many times the test what we follow in our unit is we do it six hourly unless the patient is very sick in that scenario we do abg's more frequently we put an art line and do abc which tells us about electrolytes also indirectly if there are patients with severe coherence who are on high dose of steroids then how to manage dk and hscc in such patients uh very very important practical problem uh because we can't do away without steroids and we have to manage hyperglycemia also steroid induced you know hyperglycemia is not responding to any oral hypoglycemic agents so it has to be managed by insulin only and as i said i follow the same principle if the sugars are more than 400 or around 350 400 i prefer to put them on insulin infusion in the initial phase first 24 hours we check the sugars as often as two hourly or one hourly and then once we determine the requirement we go for uh subcutaneous okay um which you told for the transition uh to check from insulin like iv to subcutaneous how much time like for eight hours or 24 hours what is the calculation uh see if the patient is unstable at least 24 hours because they don't settle down less than 21st sometimes they may require even 48 hours if the patient is very severely acidic and very severely dehydrated they require at least 48 hours to rehydrate you know if you do faster than that there can be complications because of that so 48 hours you should continue with insulin infusion by the time probably the nutrition has started dental feeding has started so it is safer to go to subcutaneous insulin next question is that that what is the dietary management of hyperglycemic patient uh in the emergency state they are usually either they are vomiting badly or they are very dehydrated the oral feeds are not usually possible if they are keto they have sometimes associated pancreatitis also they may vomit also so uh if they are able to tolerate oral feeds and they feel hungry then nothing like enteral feed plenty of fluids orally is the safest but if they don't then we have to go for uh iv hydration and by and large usually as the ketones starts coming down they start asking for food usually these are young children or young patients so they they're quite voracious eaters after that sometimes it becomes very difficult to manage their you know postprandial sugars yes and there are two three questions about potassium that if you could please explain potassium management should it be added in dns or ds containing 10 units of rapid insulin see the best way of giving potassium if you have a central line is to give through central line but if you don't have a central line then it would be you have to add it to normal saline and give it accordingly now in the initial stage as i said you have to give about 2 to 2.5 liters of fluids so that is uh giving in potassium in that bolus would be a would be very dangerous so i would prefer to have two lines one line you use for bolus and another line you use for potential supplementation but if you have a central line then you can use it a separate channel for potassium supplementation and i i give this thing a bit anything above 5.2 don't start potassium infusion 5 to 5.2 10 milligram per hour is usually the dose between 3.6 to 5 you can choose to you know 30 to 40 milligram per hour supplementation but start with insulin only after the potassium is more than 3.3 because as soon as you start insulin the potassium will further go down and these patients can have severe hypokalemia and the hypokalemic patients unless the potassium is corrected the arrhythmias will not respond what first aid should be given before the patient is referred to a hospital so to stop the progress of the condition huh by enlarge see diabetic ketosidosis patients are they present because they have skipped an insulin right so and many times these are young children they don't tell the truth because they know that they will be reprimanded many of them have several episodes they are they are aware of it what is happening they'll tell that oh no i have taken insulin so a proper history and if you have a finger stick this thing sugar checking at home by and large most of them do check their sugars and keto sticks are there then you have an idea so best thing is to start hydration at home and bring them to if they are not able to keep anything orally uh put an iv line if you can and bring them to hospital as early as possible i i would say here one thing don't hurry up to give insulin to them see these patients are not going to die of hyperglycemia they are going to die of dehydration so if suppose you are not able to reach i mean bring them to hospital as early as possible at least try hydrating them okay dr shreya is asking should police always be inserted in dka depends on the patient's condition if the patient is fully conscious you can still wait but if the patient is thick enough to the come to to come to the icu it is always better to have a folies you will have an idea of how much is the urine output a rough idea of hydration uh dr shreya we did ask ma'am what is portland protocol if you could just elaborate on exactly what you want to know about the portland protocol dr sanjeev is asking any specific guidelines for iv infusion of insulin with corresponding sugar levels it's a very controversial thing everybody is using it but nobody will agree to it the recommendation is 0.1 unit per kg per hour bolus followed by 0.1 unit per kg per r is the hourly insulin suppose the person is 60 kg 6 units of bolus followed by six units per hour and keep monitoring sugars in the range of they should start falling by 50 to 80 milligram per deciliter and if they fall more than that then start reducing it by half of it so coming to 3 ml and if they don't improve at all then you can go up to doubling it but normally normally everybody does it in a different way in the practical ways that you give point one unit per kg per hour another point one unit per kg as bolus and followed by same dose you start as hourly basis and keep checking it reduce it say you started with six ml per hour if the sugars have dropped more than 100 then reduce it by half if they haven't dropped then continue with that that is the simplest way of doing it [Music] but when you are giving high dose of insulin always keep checking your sugars because hyperglycemia will not kill the person but hypoglycemia will definitely so avoid hypoglycemia dr saying portland protocol is iv insulin management which is done in icu in emergencies but do we use it regularly this is the protocol i use i don't know whether it is called portland i am not good at names so i am sorry i do not know this name wrote a universe is asking can we still use the term iddm yes we can yes yes doctor said thank you uh i'm just trying to understand what exactly the question 1ml kcl is equal to 2maq for potassium so phosphate 1ml is how much i think he meant phosphate in mecu potassium phosphate is available i exactly don't recollect the ampoule constituents but it is written on that i mean one can always check it potassium phosphate is available with i don't remember exactly the male equivalents right now uh is it reasonable to give prophylactic antibiotics in dk and hhs see again here the answer i have already answered it the books will say do not give antibiotics unless there is a definite evidence of infection but practically i tell you it is very difficult or rather impossible to know whether there is an infection or not when the patient has come to you with a you know severely dehydrated state and is dying one must make all efforts to identify if there is a focus of infection or not it won't be wrong to give antibiotics for first 48 hours and in the meantime try to look for infection if you don't find any you can always stop it after 20 48 hours you won't be wrong most of the time which is more difficult in my opinion in my opinion see protocols should be just guidelines they shouldn't be watertight one question is which is more difficult to treat hhs or decay it depends i think hhs is more difficult difficult in the sense because it has a lot of comorbidities and usually the patient dies because of those comorbidities rather than only hyperglycemia well if you see dk usually they are young patients other systems are good and you have a lot of time to you know manage them another question is when can we start in dk patients or should we discharge patients only on insulin i am not the right person to answer this because i deal with intensive care patients i don't like to start oha in the icu only when the patient goes out of icu i hand them over to a dermatologist and then they manage by by and large dka patients are insulin dependent most of them require insulin they don't go on ohs well ma'am and we have many positive comments everyone has loved this session and i'm sure they must be clear thank you so much at around 400 rbs at what rate usually we should start with insulin infusion see at 400 normally if the sugar is 400 i start with the for 4 ml to 5 ml we give 5 5 ml 5 units of bolus and then start with 4 ml per hour how do we manage dka with low ef or acute heart failure i have a tricky situation by and large usually decay occurs in younger patients so heart failure is usually not an issue and these patients they they are so volume deprived so they tolerate 1.5 to 2 liters of bolas you know within few minutes also they don't decompensate but if it does happen in older patients sometimes in older patients you can have decay coming up in that scenario you have to individualize the fluid normal normal recommendation is 15 to 20 ml per kg bolus so say uh 60 kg person is there so around 1.2 liter of bolus you can individualize it to half the this thing and you can use ivc as a guideline or you can use the clinical symptoms as a guideline pro bnp as a guideline and determine the volumes well ma'am i think there's one more what's the maximum rate of insulin that can be given for r some patients are not responding to 0.1 mu per kg per arm you can you can double the dose well those were the questions and thank you so much man it was a very very nice session we have just the emojis flowing in the positive comments flowing in a very nice session and like you said although it's an uncommon medical emergency still the word emergency is there so when they'll come they'll come as emergent as they can come so thank you for all the diagnosis and the treatment modalities that you explained i'm sure our audience enjoyed it a lot

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Dr. Murtuza Zozwala & 1226 others

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dr. Pratibha Dileep

Dr. Pratibha Dileep

Critical Care Specialist, Zydus Hospital

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dr. Pratibha Dileep

Dr. Pratibha Dileep

Critical Care Specialist, Zydus Hospital

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