00 : 00 / 05: 00 (Preview)

This discussion has ended. Watch the recording on Medflix app,

Commonly Reported Endocrine Emergencies & its Management

Mar 29 | 3:30 PM

Endocrine emergencies, excluding the common diabetic emergencies, are rare but more significant because of their low incidence. A high level of suspicion is often required to make a diagnosis. However, conditions like myxoedema coma are usually obvious. Often, the physician needs to initiate treatment for these conditions before a confirmed diagnosis. Join us live on Medflix with Dr. Arundhati Dasgupta, who will guide you on the commonly seen endocrine emergencies and the management approach for each of them!

[Music] hello and welcome to all of our attendees today i dr fatima on behalf of team metaflix extend a warm welcome to all of you today we have the honor of having among us dr arundhati dasgupta who is a renowned endocrinologist and diabetologist currently co-founder and director of diabetes and endocrinology in the endocrinology division of drugs super speciality care at silguri mam is extremely passionate about diabeteology and metabolic disorders mam also is part of numerous initiatives to raise awareness among these topics among the masses and we're truly grateful to have you here among us today doctor hello grieving thank you for joining us tonight over to you doctor we really look forward to learning from you thank you so much dr fatima and i think this is a very important topic when you suggested this i was like yes this is one topic that we should be you know discussing it's not often discussed probably not as often as we should uh can you see this light is it visible yes well yes well right so you know uh when we talking about endocrinology let me tell you something most of us who are endocrinologists have probably chosen this subject because it doesn't have an emergency or immediately doesn't have emergencies because uh you know we are aware that the other superspecialities whether talking about nephrology or neurology or cardiology they are associated with a lot of emergencies so generally when you think of endocrinology you don't think of emergencies but the emergencies associated with endocrinology can be really really critical because because they are not that common they might often get missed in their diagnosis i mean you're not going to miss an emma you're not going to miss a stroke because you know you keep seeing them so often so there are no chances of you missing them but because of the endocrinological emergencies being much rarer as compared to the other you know counterparts in in the other specialties it is important that we also keep the threshold of suspicion low and we will you know go through a few of the common endocrinological emergencies and um because it's not really possible to touch on all of them in details in the given amount of time if you have any particular question then we can always take them up at the end of the presentation so when you talk about endocrinological emergencies the first thing that comes to our mind is of course diabetic ketoacidosis and this is you know in comparison to the other emergencies it is you know one of the uh conditions that is often faced by my practicing physicians by pediatricians by endocrinologists across um you know the practicing spectrum of anybody who's dealing with diabetes and even somebody who's not directly dealing with diabetes maybe somebody who's practicing at the phc level because this is a you know a condition which is more often seen in children at times if you're not thinking of it i have um you know seen patients who were who are presenting with diabetic ketoacidosis but because they were not known cases of diabetes uh the the primary treating physician did not think of it and you know they were thinking of all other things and a lot of things were given before that the reports came in and sugar levels came really high so that's when the you know the entire process of treatment started so basically when we're talking about diabetic ketoacidosis it's a condition which is characterized by number one hypoglycemia because of severe insulin deficiency which is either absolute or relative um as a result of which there is impairment of the peripheral glucose uptake and fat breakdown and also relative glucagon excess which promotes hepatic gluconeogene genesis the next part is about ketosis because there is a shift to the fat metabolism which leads to an increase in the feed the fatty acid oxidation forming the ketone bodies acetoacetic acid and three hydroxybutyric acid and the third component is acidosis now a lot of times you know we do get patients of type 1 diabetes with severe hyperglycemia with ketosis but without the acidosis so not every hyperglycemia or every you know child or you know adult with type 1 diabetes or type 2 diabetes at times we do see very high levels so you're seeing something to the tune of 600 650 700 and you're seeing ketones in the urine or ketones in the blood if you're getting it tested but they need not necessarily be in acidosis so they need not be you know termed as dka but to be termed as dka the presence of acidosis which basically occurs because of the dissociation of the ketone bodies is essential generally the the patient will present with thirst extreme thirst polyurea and there'll be variable levels of circulatory stress initially the hemodynamics may be maintained but later on because of you know the persisting polyurea because of the hyperglycemia the patient gradually goes into a state of uh hemodynamic collapse and uh you know various degrees of shock when you if you're attentive to it a lot of times there is the the smell of acetone and once you've heard i mean you've smelt the you know that acetone uh smell ever you're not going to forget it because it's a very typical kind of a smell in the in the bread that is because of the ass of the ketosis if you're going to investigate this patient you find um increased anion gap leading to you know respiratory alkalosis patient might often have tachy generally the precipitating causes are are conditions which require the um you know the other hormones of the body like epinephrine growth hormone and cortisol to rise and that results in insulin resistance and reduces the effectiveness of whatever insulin is present in the body either you know injected or produced in the body whatever is there that bit is not enough to cover up the actions of the other hormones and that usually happens in conditions of say infection like pneumonia or conditions like myocardial infarctions or any surgical emergencies not to forget of course the errors of insulin administration wherein for a long time probably the person has been administering the insulin in a wrong way the insulin is not getting absorbed and thereby the hypoglycemia or often a lot of times we do hear about patients manipulating their insulin treatment or stopping the insulin treatment maybe type one diabetic patients stopping the insulin treatment and going for some other forms of therapy uh you know and then landing up with dka so this is something i'm sure all of us who are dreaming with diabetes have seen where they go for some this you know therapy or other and then they land in bka so these are the common precipitating you know conditions when you're diagnosing diabetic ketoacidosis and you're looking for hyperglycemia looking for ketones in urine you're looking for acidosis remember certain catches sometimes the you know in the urine you know that this patient is typically looking like a diabetic ketoacidosis there's a the you know the ketotic breath there is a hyperglycemia there's the acidosis but when you look at the urine there is no ketone now remember the early stages of dka uh here they are unable to detect the the ketostix that we generally use for the detection and the ketones are unable to detect the three hydroxybutyric acid and generally this is usually the first or the main ketone in the urine so then is where the plasma ketones come handy but unfortunately not a lot of us have access to plasma ketones urine ketones is a relatively easy thing to do because you get those strips you can keep them and then you you can use them whenever you're required whether you're practicing at the peripheral level or the at the tertiary tertiary level but blood plasma ketones is not something which is done very regularly in all laboratories so that might be a little bit of a catchy area there but um you need to keep that in mind when you're you know you're thinking about it clinically and it's not fitting if you think that you know the dka is not the reason for the acidosis it's important to look for the other causes like you know the lactate levels in others sometimes what happens is the patients would be coming to you after being referred from certain places so there somebody would have seen the high sugar and would have injected some amount of insulin before sending the patient so you might not get as high um blood glucose as you might be expecting in these conditions do not forget about the pseudo hypotremia that could occur because of the you know highly lipid serum or because as you know for every high glucose level beyond and you would have to uh you know correct for the serum sodium by 1.6 so once you correct it then you should look at what the sodium level stands at also remember because there is acidosis the sudden potassium level might initially be very high because remember acidosis drives potassium into the extracellular compartment and as soon as you're starting treatment and the acidosis is getting resolved this potassium level tends to come down so there is a catch in that because when you're when you're practicing when you're putting in the potassium we do know that when you're putting in the insulin you would put in a little bit of potassium depending on what the potassium levels are and suddenly the potassium levels might go down so be you know be ready to be checking your sodium and potassium levels on an hourly basis when you're treating a dka the primary thing about the treatment of a dka is fluid because this is this is the patient presenting with gross fluid loss and hemodynamic collapse so you have to put in a lot of fluid but at the same time you have to be careful that you're not you know overdriving things so generally it's like one liter during the first r and if the hypotension is is persisting then you give a plasma expander and then you would decide on the the rate of fluid based on the age of the patient the other comorbidities of the patient fitness of the patient but it's generally one liter in the next two hours one liter in the next four hours and then one liter six hourly if somebody i mean if the patient is has a cardiac disease it's a milder form of dka or you know um then uh or it's an you know a relatively elderly patient then you would go slow with the fluids and once the blood sugar has reached 250 you would um switch to five percent dextrose instead of um the point nine percent uh saline and uh if also during the course of treatment the sodium levels go higher than you would switch to point four five percent saline insulin you would put in an insulin pump you do know 50 units and 50 ml um in the in the syringe and then you could start off at a rate there are various you could look up into the net for the various regimens that have been put forward you could decide your dose based on that but generally we would start at maybe something like six units per hour this point generally given say the body weight would be something around you know 50 to 60 or maybe slightly less if it doesn't come down substantially within a period of one hour or two hours you would increase the dose of infusion again depending on the body weight depending on the patient's condition and sometimes we really have to go very very high you know initially because there's this major glucotoxicity which initially doesn't allow the sugar levels to come down for quite some time and then you would see that once the sugar levels start coming down they come down quite rapidly so initially you do not get frustrated if you are putting in like six and then ten and twelve units per hour and nothing is happening the blood glucose is remaining at high do not get upset because you'll see that beyond say three to four hours or five hours then things start moving into uh you know place and then gradually the levels start coming down and they you have a lot of scales by which you could gradually titrate the doses and once the patient is at the bicarb level is normal the patient is eating and drinking you could and has been on insulin infusion for at least 24 hours you could shift the patient to sub kidneys insulin do not generally wait for the urines to become you know free of ketones because that could take quite some time and you know it's not necessary to wait for that long how long uh what is the dose of the subcutaneous insulin is again going to be decided there are we cannot go into the details out here but there are a lot of ways of deciding on the doors you look at the last four hours of insulin requirement of the body and then you extrapolate that to 24 hours and then you divide into basal and boneless doses according would you be using bicarbonate initially they were used a lot but these days we generally do not use bicarbonate in dka in spite of the acidosis because uh we are concerned about the potential harmful effects like hypokalemia and arrhythmia and you know cardiac irritability discomfort um though these can be uh slightly uh you know better with the use of bicarbonate all in all we generally choose not to give bicarbonate unless there are certain specific conditions again which can be discussed later on so the other uh presentation of hyperglycemia is the hyper glycemic hyperosmolar state or honc now this is again characterized by hyperglycemia with high plasma osmonality and ketoacidosis is generally absent or less marked so as very high sugar levels ketones not their very trace no acidosis high plasma hospitality usually in a patient of type 2 diabetes usually in the elderly gradual onset and this is what you know clinches the diagnosis of fiber osmolar non-ketotic coma there is usually a an underlying condition that has exacerbated this and here the blood glucose that rise unlike decay has not been sudden it has been slowly over a number of days and patient has been you know will complain of not having uh felt very well or have no has not kept very well in the last one week or ten days and um here we because there is no ketosis because there is uh usually enough circulating insulin and um so thereby there is no acidosis also because of the ketone emia but sometimes when these patients are very sick you might have lactic acidosis serum hospitality is is is usually very high and it can be measured in the laboratory also it can you can measure it by you know the formulas you know using the sodium potassium and glucose levels and then you could calculate the ceremonity and if you see that yes yeah this fits into uh you know as condition with high hospitality high glucose patient is it could be could be irritable could be um having the sense of unwellness could generally patients do not present in coma though the term says honk they generally do not present in command list like they have been in that state for quite some long time we do see some patients presenting with uh you know focal seizures in fact vocal seizure has been something that i've seen quite often with honk patients and then once you correct the sugar levels and uh you know maintain the fluid and everything then patients uh recover from that the neurological manifestation also uh treatment is generally the same as that of decades about you know the glucose correction but here the fluid requirement is is lesser and you could use um you know fluids based on you would naturally these are elderly patients they could have other comorbidities so you'd have to decide based on that but once you start replacing the fluid the blood glucose levels also start falling down and then you could decide on the insulin replacement initially of course here also you'd be putting on a a pump but later on you could gradually shift to continuous insulin hypoglycemia uh the most common endocrine emergency if you if you place it that way we do know because of inadvertent dose overdose or you know somebody who has missed a meal or suddenly started an exercise regimen or underlying factors something like addison's disease or renal impairment or hepatic impairment or severe sepsis coming and that could cause a symptomatic hypoglycemia we are aware that hypoglycemia generally would present with you know autonomic and neurologic symptoms and you your patients have sweating anxiety nausea palpitation this is what needs to be told to the patient because a lot of times you know they will not reach you during the condition of hypoglycemia and they could well have other things like say drowsiness or fatigue or cognitive changes now talking you know irrational behavior and eventually could lead to seizures and and also coma so uh also focal neurological deficits that mimic stroke at times um are found in in presentation uh with uh you know patients having hypoglycemia and a lot of times they go through a lot of investigations before actually hypoglycemia is thought of because um sometimes maybe there's nobody to give the history or sometimes you know the history is heard but it's not you know looked into a lot carefully so though it appears odd i mean we do see patients we've heard um you know these patients who were having these symptoms they went to the hospital they got a ct done and a lot of investigations and the blood sugar was done but then it was missed you know it was missed that the the report was not seen or maybe somebody who just checked did not realize what he was uh i had a patient where the you know the the sister had seen that it said low but she assumed uh you know she thought that probably the battery is low and then she just didn't care didn't tell the doctor and he was busy doing attending a lot of other patients in that emergency so this patient stayed in hyperglycemia for quite some time before the doctor came and rechecked again and found this error so now this has to be there in the minds of everybody the patient the attendants the doctors the nurses the people who are attending to these emergencies in schools where who are dealing with type 1 diabetic kids so that's why when we do these awareness programs we also tell them it's not only for you it's also for the other people that you could be seeing so that you can identify these problems obviously if the patient is in a condition to eat you put in oral glucose if the patient is not in a condition to eat you will put in iv glucose if the condition is like very serious and venous axis is not available you could put in a glucagon subcutaneous or im but generally the patients recover very soon uh with 25 dextrose and that's how that would have to be dealt i'm sure all of you deal with hypoglycemia and this is not something that we need to uh you know uh speak in general because a lot of you would be knowing about hypoglycemia but i have seen uh you know conditions where these are mystals inadvertently but these are missed also i had once done an opd with um neurology residents and we were like looking the patient's a patient's coming and saying that i i'm feeling dizzy i feel busy during this part of the day and they were thinking of like okay he feels dizzy at this part of the days it's something else within your mysteria and a lot of other things but they were not thinking of hypoglycemia so when i was hearing because i am my youngest student to think of you know my mind is due to thing of hypoglycemia their their mind is due to think of the neurological problems so immediately i said this is hypoglycemia and when they you know got the patient tested and an smbg was done it was diagnosed so that's it i mean we should keep this in our mind i know for an endocrinologist i this is the first thing that i'm going to think but when there is somebody who is dealing with the gynae problem the pediatrics problem the medicine problem this might not come to your mind immediately so we just need to you know keep telling ourselves okay so these are the general things that diabetic patients might present with in an emergency condition thing that i'm going to talk about is pituitary apoplexy it's not you know as common as in the as the emergencies in the in the diabetic setting but uh again i'll tell you one of uh uh my um you know experiences so this was when i had joined um a corporate hospital and uh so this a patient had presented in um at night so he had presented with um a headache and he had presented with loss of consciousness so and he this was a patient who was a known case of pituitary tumor non-functioning pituitary tumor for which you know uh it was he was advised surgery but he did not get it done because he said it's not causing any problem i'm not going to go ahead and do it and then he landed in the emergency now uh the emergency doctor saw him got got all the investigations done uh but he did not do the serum cortisol obviously so the patient he had put the patient on the bp was down so they put the patient on expanders they put the patient on uh normal slime and um yet you know it was not rising in the patient on dopamine they did not give the patient steroids because they were not thinking about this right in spite of the diagnosis glaring at them on the face so uh next day when i was visiting the emergency to see one of my patients and there was this discussion so i just looked up and they told me that look okay this guy also has a pituitary adenoma can you just have a look and then i was like oh my god this is like a pituitary apoplexy so and then i asked did you get a serum cortisol done and they said no and uh when we got it done you know then of course the levels were very low this was um and there were hemorrhagic features in the pituitary tumor which was which again the resident on duty did not know how to see and because it was at night and the radiology had been reported to them so till the morning hours which was almost like 12 hours after the patient had got admitted the patient was did not receive the steroid and on giving the steroid the patient you know remarkably improved because this was basically a pituitary apoplexy with severe hypercortisolism which did you know improve which generally improves when you give put in the steroid so it's it's it generally occurs when um there is infarction or sudden hemorrhage of the pituitary gland associated with the with the previous pituitary adenoma though it can also occur in a normal pituitary gland say like condition conditions like she hands when there's major bleeding you know there's major hypotension and infarction of the pituitary that can occur and uh while incidentally found hypoplexis is more frequent than acute but around 25 percent of all tumors generally you know display hemorrhagic or infarction features it's very rare obviously as you can see the numbers it's very rare but 2 to 12 of the patients with adenomas experience apoplexy so that needs to be kept in mind precipitating factors have been reported such as you know some procedure some surgical procedures some head trauma pregnancy somebody on anticoagulant therapy though that's very rare uh but that can also incite about pituitary apoplexy and sometimes very rarely again dynamic testing so you were assessing this patient for uh for you know the hormonal aspects and you did a dynamic testing and sometimes that could also result in pituitary appropriate see clinical presentation is generally varied it can be as mild as just a little bit of headache or as severe as coma with like visual disturbance the presentation of pituitary deficiencies with acute onset blindness coma and hemodynamic instability in between so one in this mild headache the other in this coma and you have a lot of other things in between but headache is generally the most common uh symptom occurring in 80 of the patients and it's a it's a very severe kind of headache which is generally retro orbital but it can be by frontal or diffuse also and visual disturbances are also quite common affecting more than half mass effect or the abrupt pressure caused by the apoplexy can cause uh sudden visual defects because of the superior extension with the compression of the optic chiasma and meningeal irritation can also occur from the extravasation of the blood or the necrotic tissue into the the subarachnoid space they could be photophobia nausea vomiting meningious so generally you would need to you know rule out other causes which might present with similar presentations and diagnosis is generally with the help of corticotropic deficiency which is present in 60 to 80 percent of the cases though other pituitary defects may also be seen but they generally need to be addressed after the acute cortical drop deficiency is resolved the acute neurological problem is solved sometimes you might have a diabetic insipidus which is rare but um it can be masked by the secondary adrenal insufficiency that has to be remembered so uh diagnosis the differential diagnosis is basically subarachnoid hemorrhage and bacterial meningitis with the kind of symptoms lp would have limited utility because the rupture the irritation caused by the rupture of the necrotic or hemorrhagic tissue can also cause a similar uh feature like pleocytosis or increase rbc or xanthochromia in the csf so generally you would need to do a csf culture if you're thinking of bacterial meningitis and you would require to do all the endocrine testing but treatment should not be delayed if you've thought of pituitary apoplexy you know all the time that you're losing in diagnosis could have an implication on the ultimate you know outcome of the patient so if you're thinking it send the blood uh samples for testing but start off with your treatment neuroimaging can be done ct is diagnosed you can only 21 to 28 percent generally you know as most of the cases have a hemorrhagic component that can be seen by the ct or else you go in for mri which is a much more superior modality for treatment of pituitary epoplexy because you could you know detect the fresh blood there and you could confirm the diagnosis in over 90 of the cases and um the early signals in early changes include the increased signal intensity on diffusion so there are a lot of pituitary apoplexys course where you could put in you know your patients features from level of consciousness visual equity visual field effects and ocular parasites and you could score them accordingly to you know diagnose and then uh decide on the management so management is either going to be surgery or you could just go for a more conservative medical management so somebody who has um you know acute presentation a severe presentation there you would think of surgery and that's about resecting the apopletic uh pituitary mass with the goal of resolving the neurological visual defects and sometimes what happens is there will be bleeding and there'll be shrinkage of the of the apopletic pituitary adenoma so you could go for a little bit by the time they come to you that would have shrunk and the clinical state would have also improved slightly so you could go for a conservative approach in these cases again based on the grading that would help you decide on um the approach to be taken so anybody who has hemodynamic instability reduced visual equity severe visual field defects or severe hypotension their empirical corticosteroid replacement should be put in and then you go on with all the investigations and others remember these are patients who will need long-term hormone replacement because um the pituitary mass would have you know been damaged by the apoplexy so the functional pituitary tissue that would be left behind could be quite less so you know they would require hormonal replacement generally coming to another area where uh and you know an endocrinological emergency could present is the adrenal and and we are talking about the adrenal crisis so when do you get a patient with adrenal crisis when during an acutely stressful event a patient who has an underlying adrenal insufficiency fails to mount a normal physiological response so you know it could be something as simple as a normal gi infection so we anybody who has an underlying adrenal insufficiency when diagnosed should be told about the increased need of the steroids during any condition of stress so any precipitating event which requires an increase in the serum cortisol level uh in the cortisol level by the body and the body is unable to give that amount of cortisol is when an adrenal crisis can be precipitated so you know conditions like a very very uh you know conditions where you would not think about um adrenaline surgery for example flight delay the the stress that is built up during a flight delay or even something as simple as a vast bite has been known to precipitate um you know adrenaline crisis even even emotional stress periods of emotional stress that has also led to precipitation of the adrenal crisis so that needs to be kept in mind patient presents with severe gi symptoms nausea vomiting muscle cramps hypotension and all of us again i would say that who are treating adrenal insufficiency we need to tell our patients i last week i had a patient who had it written in all his prescriptions that you know when you have if you have loose motion or fever or cuff please double your doses and this participation has been seeing me for for five years or so now and yet he landed up in the emergency because he had lose motion he forgot about this thing that he had to you know double his doors and he reached his he stays in a rural area where the person didn't really understand for quite some time till his son who suddenly remembered this thing got back his prescription showed him and then the adequate action was taken so we will need to reiterate with our patients again and again because they might forget and that could land you know your patients in absolute uh difficult positions particularly if they are not uh in you know they are not in a position where they if this condition could get identified and treated because all it requires is just the steroid injection and the patient is up in the mouth but neurological manifestations could alter the mental status the patient could present with delirium they could be hyponatremia they could be convulsions myopathy contractures and sometimes patients can land in coma which can be fatal as such generally when you're getting the you know blood test stand this is our case of hyponatremia with hyperkalemia you could have a rise at the bu and because of the pre-adrenal failure hypoglycemia and hypercalcemia are other features diagnosis is again with the low cerebral cortisol and low or all the other laboratory features that we saw if possible draw the blood keep it i mean send it for cortisol and ecth and aldosterone and others but start the treatment once you've drawn the blood test for the precipitating cause whether it's an infection or anything else fluid resuscitation and steroid replacement on the main therapies prompt rehydration is needed and careful monitoring of sodium is also required now once the patient is stable you can taper it down the injectable and then you know mineral corticoid has to be started when the dose of hydrocortisone falls below 50 and then you could shift to oral so we will need to rush into the other endocrinological emergency which again is something which uh if you know the diagnosis it's very easy it's it's you know to put in the scores and then you know say this is a thyroid storm but so many times the thyroid storm is missed because firstly these patients are not a lot times identified or known cases of hyperthyroidism so and they land with palpitation they land with you know fever they are agitated so they land in various places they might land with the physician with fever they might land with the cardiologists because of palpitation they could land with the gastroenterologist because if it's lose motion or anorexia or you know rising liver enzymes they could land in the psychiatric department because they're extremely anxious they have tremor and though it seems really funny that you know this this is a condition which is almost written on the face with the patient walks in but if you're not thinking of it you could miss it so many times so uh they have a lot of you know they have high fever out of proportion to an infection diet they're sweating a lot they have tachycardia they've got tremor we should be vomiting nauseas diarrhea and severe cases could present with jaundice again they could have agitation emotional ability confusion psychosis and eventually coma and they can present with seizures or you know status also yes uh somebody did say pulsar and irregular yes so these are if you can you know you could just zoom in and have a look or this is a scale which you could be getting at the net also you could just keep it handy because so that if you fit in the the values look at the pulse rate and looking the temperature and the you know presence of heart failure or not the gi symptoms and you could yeah if you're looking at the cns the precipitating event and you could just put in this course there and anything as you can see there if you just look at it you can zoom in and see that anything which is more than 45 says that yes this is a thyroid storm 25 to 45 is about impending storm and less than 25 is about yeah the you know it you could think uh uh okay uh right i'll try doing that the next time sangeeta yeah so less than 25 is that the storm is unlikely how are you going to diagnose you're obviously going to have a hypothyroid picture uh but you know not all hyperthyroid patients are in thyroid storms so that needs to be understood whether the patient is just in a thyrotoxic state or is the patient in the thyroid storm because treatment could be a little different and based on whether yeah whether this is thyroid strong or just thyroid toxicosis basically your treatment is going to be about inhibition of the new thyroid hormone synthesis wherein you're going to put it you know carbohydrate proprietary uracil inhibit thyroid hormone release that could be done with lithium or sodium iodine or block the peripheral effect with beta blockers or enhance the clearance with cholesterol and this is something that we really do but the other three we put in acetaminophen may be needed external cooling may be needed fluid resuscitation stress dose steroids to prevent the adrenals insufficiency as well as decrease the peripheral conversion and remember that in spite of the best of diagnosis and intervention it has a very high mortality rate a lot of times from cardiac causes so yeah propranolol iv yes beta blockers we were talking about that yes we could put in propranolol iv also a lot of times we put an oral also we put it to the right steve also depending on the condition of the patient your setup you could decide on which mode to put in but you could use ib as well as oral and diagnosis as we said it's it's like um you know you're going to find um yeah so you're going to find a low tier such a high t3 t4 but uh again do not depend on that i do not know about any rule of homeopathic medicine because i know don't know anything about homeopathic medicine there's somebody who's asking that and treatment as we said is is is also about area protection and uh in the west they do put in iv uh lt4 also but we do not have access to iblt4 so what we do is we put in uh huge doses of oral default through the rails tube initially around you know five tablets 100 mcg and then gradually follow it up with 100 mcg daily it's not possible to go into the absolute details of treatment because you understand we need to cover so many other things also uh the other uh the diametrically opposite thing mixoderma coma that's like again mixodoma coma a lot of time mist because it's not thought of and uh it has a very high mortality rate of 20 to 30 percent generally triggered by systemic illness in a person who is hyperthyroid may have been diagnosed or may not have been diagnosed earlier on any infection uh something like a stroke a trauma and cold winter months is when you see a lot of nixodemocoma and it's more common in the elderly more common in women because thyroid disorders are more common in women but younger people might also rarely present with pixederma pixitamacoma current features depressed mental status hypothermia which can be very severe dry brittle skin you know dry skin non-pitting edema hoarse voice macroglossia delayed reflexes hypotension shock ready arrhythmias and prolonged you know mechanical ventilation is a lot of times needed because of the severe hyperventilation gi bleeding sometimes uh they can also be seen neurological manifestations are like very common you could have depressed mental science cerebral signs and up to 25 of the cases and sometimes they might not you know present with frank oma but generally they're this like you elderly patient who's confused and a lot of times you know you're not thinking of mixoderma coma you're thinking of a lot of other things the patient would be taking some sedatives that could have led to this and uh so whenever you see that kind of a patient an elderly patient who's like has hyponatremia has has hypo or you know tension has hypothermia think of the thyroid first or as an altered mental status think of the thyroid and do get a tsh level tested at the esogen t4 tested and this is what we just said that sometimes an lp is done so there'll be an elevated csf protein uh pressure with an um elevated csf protein level so and then again you could be um yeah you know that diagnosis thinking of something else and not mix it in my coma so remember to get the thyroid test done and lastly before we go on to the question answer session we'll go we'll talk about the pheochromocytoma crisis anybody who's seen a few prominent atomic crisis is not going to forget it anytime soon because this can be really really uh difficult to deal with these patients uh if we talk about it it's basically caused by the unopposed high circulating levels of catecholamines at the adrenal receptors the alpha receptors which cause a pressure response causes a rise in the bp beta receptors has a positive ionotrophic and chronotrophic so you have acute hypertension and you have tachycardia a severe tachycardia there's severe headache there's diaphoresis so patient is presenting with palpitations sweating severe headache anxiety tremor and could have a pulmonary edema in a presentation of pulmonary edema nausea vomiting abdominal pain paralytic alias hyperglycemia altered consciousness myocardial infarction and these are periodic effects and they build up over a few minutes and then they fade gradually so uh you know over they last for about about 15 to 20 minutes or sometimes it's very rarely they can be sustained but generally you would need to think that it's going to build up stay for 15 20 minutes and then you know gradually fade out and you could also see the presentation with the end organ damages like hypotensive retinopathy or left ventricular hypertrophy or renal impairment or proteinuria and these could also be the presenting the features do look for the other conditions to rule out the other associations like neurofibrim and cafe olay and these are the other risk factors that are associated that has been shown you could just look it up men neurofibromatosis von hepalindu these are other associations biochemical diagnosis is is about estimating the 24r free catecholamine and metanephrines a plasma metaniferance may also be used it's important that the 48 hours of alpha block it precede the beta blockade because you do not you know if you do not block the alpha receptors first there could be an unopposed action in the catecholamines of the alpha receptors so you could start with you know very these are conditions which have to be definitely dealt with by people who are used to dealing with them because otherwise you know it can be very difficult but it's important more i would say then to treat is to diagnose these patients so that once you diagnose it you will you will know what to do there you would have to use long acting alpha agonists like you know doxazosin or calcium channel antagonist and labitolol is used much later once the alpha blocking action has already set in so when we are talking about endocrine emergencies we oh i'm so sorry the others oh there seems to be some we are talking about a lot we are talking about diabetic ketoacidosis hyperosmolar coma hypoglycemia adrenal factors adrenal crisis geochromocytoma thyroid you know thyroid storm mixoderma coma and pituitary apoplexy there are others like say acute hypercalcemia hypocalcemia but we cannot go into so many details so we have tried i have tried to you know discuss all these points in general now if you have any questions i'll be happy to take thank you doctor aaron ruddy i'm sure everyone here agrees that was indeed enlightening mom we'll just give a moment to our audience to put in their questions we already have a couple of questions just giving a minute more doctors you may also click on the raise hand uh feature to come on state and directly direct a question to dr arundhati shall we start the questions okay dr asmitha has asked in the case of suspected adrenal crisis if the steroid was given empirically then when can the biochemical testing be done afterwards so generally if you're thinking of adrenal crisis and planning to put in this strata just take a sample don't you know just just let it go take a sample and then put in the um you know injection of the steroids if however um that you know somebody had forgotten to take the sample then do not take it any time soon let the patient recover from the acute phase once the hemodynamic stability is maintained patient is good you know doing well you put the patient on oral steroids patient is you know comfortable otherwise is when you're going to see so it's more if you've not taken the sample immediately i mean you need not really stop the steroid later on because unless you stop the steroid for like 24 hours or so you would not depending on which steroid is being given but like you would not get a proper result with the serum cortisol because it would be suppressed unnecessarily so you would not reach a diagnosis so what you do is allow the patient to become stabilized put on oral then you know just shift to confirm that yes this patient did have a low uh serum cortisol to start with we also have a question from one dr ritwik pam how to manage hyponatremia in mixed immunocoma so you would not be managing hyponatremia in mexico per se because this is remember this is more about pseudo hyponatremia so here what you would need to put in is more importantly the thyroid replacement you would put in the hydrocortisone replacement you would put an adequate fluid you're not going to treat hyponatremia per se as hyponatremia now if this is mixed in my coma when you're going to you know start this thyroid you're going to start the steroid you're going to put it in the fluid the hyponatremia is going to get dissolved on its own generally you would not need to put in anything else extra for the hyponatremia okay thank you mom thank you for answering the question we also have a question from dr akshata dr akshita wishes to know the role of anti-tpo antibodies in diagnosis and treatment of thyroid stomach i think so anti-tpu is is something which just tells us about the cause that is the autoimmunity part of it so anti-tpo antibodies not something which is going to help you diagnose a thyroid storm you know a thyroid storm is on clinical features and thyrotoxic present you know uh the rise in t3t4 and the fallen tsh with the clinical features whether this is an anti-tp of positive patients i mean whether this is uh it could be a graves presenting with um thyroid storm but you could also have a toxic montenegro representing with the thyroid so where you in that case it would be probably anti-tpu negative because unless you consider that around eight to twenty seven percent of the operation as such the identity positive so do not look at anti-tp at that point in time it's not going to help you anti-tpu when do you do an anti-tpa when you want to cleanse the diagnosis when you're you know you want to find out whether this is graves you want to find out whether this is hashimoto's this is when you go ahead and do the anti-tpo this also helps your diagnosis same sub clinical hypothyroidism you will do an anti-tpu to decide whether you're going to treat that patient or not in pregnancy uh you know you would want to probably do an anti-tpo in hypothyroid patients or otherwise to to understand about postpartum thyroiditis the chances of going into postpartum thyroiditis but not in an acute setting like a thyroid storm okay thank you mom uh dr ritwik has also asked can dexamethasone to be given in an adrenal crisis yes it can be given in an adrenal crisis yes that this is i mean you're going to give it examination adrenal crisis you could choose hydrocortisone or you could choose dexamethasone okay thank you mom a question from dr nishmita are can pity apoplexy eventually cause empty cellar yes it can it it it is in all likelihood going to cause empty cellar so that is the reason why these patients are you know generally have to be on long term uh pituitary hormone replacement because a lot of times uh whatever remnant tissue is less left behind will not be sufficient to you know provide all the hormones so they might not have all the hormonal deficiencies but they might land with some of the hormonal deficiencies yes okay i hope that answers your question dr nishmata dr sanjeev has asked diagnosis and management of pheochromocytoma at unusual sites difficult because if you do not have access to a lab which does 24 hours you know urinary cataclysmins how would you diagnose it so i i it's no use saying that yeah you do this and you do that but it's difficult that's why i said that um you know a few chromocytoma can land in a very even in medical colleges we've had trouble dealing with theochromocytoma crisis because um because they landed in medicine or they landed in the eye department with an acute um visual impairment and then the bp was checked and then over a period of time so you have a team it's easier to deal with it if i see that at the peripheral level you can diagnose and treat it'll be very difficult i'd say if you suspect it send the patient to a tertiary level where a team effort can be you know put into practice okay mom dr anuj wishes to know please tell us more about subclinical hypothyroidism treatment so subclinical hypothyroidism treatment is generally given in certain conditions not in all and we were talking about anti-tpo so anti-tpu positivity is a condition where you would go ahead and treat hypothyroidism uh pregnancy is another condition where would treat subclinical hypothyroidism or maybe the patient has subclinical you know levels maybe something like seven or age but has um clinical features or has symptoms which are very suggestive of you know hypothyroidism say um severe fatigue or dry skin or or hair loss or a history of menstrual irregularity that is when you would treat subclinical hypothyroidism or in the elderly sometimes if you have the severe constipation generally in the elderly choose not to treat hypo you know subclinical hypothyroidism unless it reaches like 10 or 15 but some times you know when there are symptoms that could be the fallout of subclinical hypothyroidism you choose to treat or something like say dyslipidemia which which could be conditions associated with hypothyroidism that's when you treat itself thank you ma'am the next question from dr dipanchu singh please tell me the prognosis of parkinson's disease diagnosed very early stage i think that would be a question that you would be asking a neurologist because the last time i've seen parkinson's so i think you would be i mean a neurologist would be a better position to answer this question yes no worries uh also a question why alpha blockade is done followed by beta blocket infused chromocytoma so if you if you do go ahead with the beta block it earlier there will be an unopposed action of the catecholamines on the alpha receptors and that is where you get all the alpha adrenergic symptoms so we should land in a severe you know crisis state so that is why we first need to block the alpha and then go ahead after say 24 hours of blocking of the alpha receptors right with the 36s then we go ahead and run beta because the beta symptoms are not going to be that severe the alpha symptoms are going to be much more severe if they're in an unopposed condition okay we have a lot of questions coming in a lot of positive comments as well uh dr ashok asking which antihyper antihypertensive in fiochromocytoma preferred one so as we as i said uh you would choose a maybe a long acting calcium channel blocker and an alpha receptor blocker which also would depend on your availability of what you have correct i hope that answers your question dr ashok um also a question regarding treatment of hypothyroidism in adolescent girls mom so hypothyroidism in adolescent girls is hypothyroidism in any phase of life is generally treated based on certain principles i mean if this is primary hypothyroidism and uh you know not subclinically hypothyroidism with the tsh has gone beyond 10 and there is there might or might not be a low t3 t4 levels you would choose to supplement with mt4 and generally we choose the dose based on the body weight and it's generally 1.6 mcg per kg body with that is the starting dose however if the tsh level is like say seven or eight or you know when you start see the patient has adolescent girl has present presented with menstrual irregularity with the presence of subclinical hypothyroidism probably you would treat that if you're not finding any other cause for you know maybe ruling out after ruling out all other causes then you would treat that then you would probably not start it as higher doses 1.6 you would go slightly slow uh but otherwise it's it's just as anything else you you start treatment you monitor the tsh levels after two months um and then you see you would your target would be to give it between point five to two point five generally or three and then you gradually titrate your dose accordingly nothing grossly different as when you know as what is done in the others correct thank you mom a question from dr gouache can we do random plasma aldosterone if we are suspecting primary hyper aldosteronism in a young resistant hypertensive without going for a ns bolus for sampling yes you can not a random you would need to do an early morning uh you know uh sarah maldonado students and you would you know do the plasma meridian activity also because it's generally the pac-pra ratio that would be clinching the diagnosis rather than only a plasma analysis concentration it's not necessary always to put it it's not possible also to go on you know go ahead with the saline infusion and then go ahead a lot of times we are doing it um you know early morning samples are being taken uh but you would need to know that the patient has given it to the supine position or in the or and you would need to mention that yeah when you're sending it across to the laboratory so they would know how to interpret the result i hope that answers your question dr gohash we also have a question from dr pallav mishra mom he wishes to know about you glycemic dka and management so eu glycemic decay has has come into a lot of discussion after the use of sgl2 inhibitors now this is a condition basically dke is a condition where there is an imbalance with between insulin and glucagon we just need to understand that and hyperglycemia is is is one of the presentations because there's the insulin relative deficiency of insulin so that's the reason of hyperglycemia and you have some some molecule which is controlling the hyperglycemia otherwise is when you're landing up with eu glycemic diabetic ketoacidosis where because of the imbalance the ketosis is that the acidosis is there but because the hyperglycemia is getting managed by something else so hyperglycemias management is is as with you know if you just leave the less the insulin portion now the rest of it is the same it's it's about correction of the acidosis correction of the fluid you know the fluid deficit that occurs because of this so it's basically about iv fluids and acidosis correction as in in in dk without that much of emphasis on the insulin in you know because generally the patient is eugenic however remember because when these patients are presenting with you glycemic um ketoacidosis because once they suppose this is because of the drug called sg to inhibitors you're taking with hdlt to anybody stopping it in the has blood levels also with so there you would need to put in the insulin after a period of time so you need to remember that also if it's because of these drugs mom we have a couple of more questions i hope you're not taking too much of your time would it be okay if i address them just couple of women thank you so much uh we also have a question from dr dipanju singh long term ohas like stl to blockers that increase urine glucose may lead to uti someday later would it be possible mom so i didn't get you uh yes yes yes are you asking whether the hdtv can cause youtube yes yes that is one of the problems with these glp2 inhibitors that you know because of uh the as you just said because of release of the glucose in urine a lot of times they do land up with utis and it's imperative that when we are using these medicines we tell our patients that they need to maintain the genital hygiene the water intake also should be adequate so you know they're flushing out and um genital hygiene is a very important area and we also need to tell them did we get any of these signs and symptoms do get back to us uh a lot of times we we have to we first time the patient presents with uti on an sdl220 maybe we would choose to put the patient on um some antibacterials or antifungals but this if this is recurrent then at times we have to stop the hdl2 inhibitors in spite of you know there being other benefits with it so yes uti can be a problem with these images at times okay uh and for how long we should be using them um dr d pancho asks using i'm sorry using what is going to do images yes yes ma'am you can use them for as long as you want as long as you know they're not causing a lot of problem okay i'm just last one question it uh it's one of the earlier questions that came by so dr charlene asks could you tell us more about the unawareness regarding hypoglycemia what can we do to make it better okay so hypoglycemia unawareness is generally a problem with people who keep getting hypoglycemia on and off so it's kind of like the body gets reset into a position so generally you would expect that you know when the sugar levels are coming down from from 90 to 80 to 70 gradually they get starting to get those symptoms the adrenergic symptoms the neurologic symptoms right but a person who's getting hypoglycemia on and off on enough his body stops responding with these symptoms and that's when you get the hypoglycemia unawareness so the treatment for hypoglycemia unawareness is to prevent hypoglycemia for a considerable amount of time so you you you know you have these patients who are coming to your opd and they have blood sugar levels like they're absolutely stable they're talking to you and they just say i'm not feeling very good i'm just being a little uneasy and you see that the blood sugar level is 35 or 40 and you're left wondering like how is it possible right so this is hypoglycemia unawareness the same person if you maintain this person i mean in a uv glycemic state or maybe slightly in the hyperglycemic range without allowing him or her to go into hypoglycemia for quite some time you will see i have had patients who now they whenever they get sugar levels of say like 80 or so they become symptomatic again so it's about resetting the threshold um it is what you generally have to do with you know hypoglycemia okay thank you so much doctor i hope this answers all your queries doctors any further queries maybe we could compile them and send it across to you at a later date mom thank you so much for joining in today we indeed had an enlightening session and i'm sure everybody here in the audience agrees thank you so much doctor thank you so much good night ma'am bye-bye good night bye-bye thank you again you

BEING ATTENDED BY

Dr. Murtuza Zozwala & 1369 others

SPEAKERS

dr. Arundhati Dasgupta

Dr. Arundhati Dasgupta

Consultant Endocrinologist & Diabetologist | Co-Founder of the first comprehensive Endocrinology and Neurology OPD clinic of the region named Rudraksh Superspeciality Care | Director of Diabetes and E...

+ Details
dr. Arundhati Dasgupta

Dr. Arundhati Dasgupta

Consultant Endocrinologist & Diabetologist | ...

+ Details

About Medflix

Medflix is a new platform by PlexusMD, India's most active and trusted doctor community. On Medflix, you can discover live surgeries, discussions, conferences and courses from some of the top doctors and institutions across the world. Join clubs in your areas of interest and access hundreds of amazing live discussions everyday.