Rabu, 12 Juli 2017

osteoporosis infusion

osteoporosis infusion

[music playing] so just to give you alittle bit of who i am, my name is christina megal. i am a registered nurse. my background isemergency nursing. i was an er nurse for 12 years. and then a year ago, i becamecertified as a wound and ostomy nurse. so i currently work atfroedtert and community memorial

on the inpatientwound and ostomy team. but i also teach for them. i teach the traumanurse core curriculum. and i'm acls faculty. and i teach that for bothfroedtert and aurora. so like mark, i have oneof these schedules that's, who am i today? and where am i working? and then i wasrecently hired to be

part of the faculty at alvernocollege in their nursing program. so i'll be startingthat this fall. so again, little bit ofeverything everywhere. but i've stayed connected tothe emergency nursing, emergency medicine world through teaching. and i'm certified, nationalcertified, since 2001 and have maintained thatcertification as well. well, we have the morningtogether, mark has informed me.

so we are going to startwith everybody's, anybody have a great love andpassion for endocrine? little bit of a hand. i know. it's one of those reallytough, tough specialties. because it's not outwardlyobvious as to what's going on with a person. and it really requiresa significant skill in that physical assessment,in history gathering,

to start to put thepuzzle pieces together. so i know you guysare all experienced. you all have a great book. and when i put togetherthe talk for this morning, i really wanted tofocus on case studies. because i think realpatient scenarios really bring this stuff to life andcan paint the picture for us of how you can have trueendocrine emergencies. we all know people whoare diabetic, right?

someone, some extendedfam-- maybe a family member, extended family,friends, or whatnot. and there are a lot of peoplethat manage their diabetes well and never end up inthese situations. but then we're going to havesome undiagnosed endocrine situation going on. you're going to have thatundiagnosed diabetic who is near the brink of comaor in a coma related. and we need to knowhow to respond to them.

so that's wherewe're going to start, if that's all right with you. all right, since we are doinga case study format, what i would like to do is i'mgoing to pass out an assessment worksheet. there are eight casestudies altogether. so on the front and theback of this worksheet, there are columns for you to jotdown data about these patients as we go through theassessment of them.

let's jump in. any questions right off the bat? all right, so in yourtextbook, of course, these are all the differentendocrine emergencies that are listed as importantto have knowledge of. so they're divided up. we've got all thedifferent types of diabetes andcomplications that can be associated with those.

we've got then the pituitaryproblems, things related to either pituitaryhormones that are going crazy fromthe pituitary gland itself, or what i seen radiologyis a fair number of people who have tumors, say in theirlungs, that actually secrete neurohormones andcause a great deal of problems. so we'll look at those. adrenals, those arealways mystery ones. that's where ourepinephrine comes from

and our mineral corticosteroids. so lots of problems with peoplewith adrenal issues, thyroid. thyroid has a great deal ofimpact on the cardiac system. so we'll look at theimpact on the heart. and you kind of startto put that together. you've got somebody who'sgot some cardiac issues, or maybe they've got alittle thyroid crisis going on at the same time. so objectives, justhave to, always

have to put those in thereto be a good educator, right? so really, the whole pointis to use these case studies to explore some of theseendocrine disorders in hopefully an interestingway, because it is a tougher subject, use assessmentto start to narrow down what the problemscould be, look at each of those endocrinesystems a little bit, talk about that pathophysiology,and then identify those therapies thatthat patient needs,

either pre-hospital or whatyou can anticipate once they get to definitive medical care. all right, so let'slook at case number one. 911 call comes in. we've got mom a little bithysterical on the phone. she says her six-year-oldson is not responding to her. and she's hysterical. she's got to help me, helpme going out on in the call. so we're working witha good dispatcher.

they alert you to the call, sendthe message out to your rig, and works to get a little bitmore information from the mom. what we find outis that mom says her son has been illfor the last 24 hours. he's been very fatigued,tired, just not his normal energy level,which is unusual for him. he's had vomiting,abdominal pain. and dispatcher's alsoable to ascertain that mom thinks that he's hada lot of increased thirst.

and she notices him running in,coming in from playing outside and running thebathroom all the time. she wasn't quite sure whathe was doing in there. but she knows he's been inthe bathroom more than usual. also been eating everything,everything in sight. and she just attributedthat to being a growing boy. that's that initialinformation we have. past medical history, none. full term at birth,no complications.

does seem slightly smallfor the age when you arrive and you first getthat first eyeball look at the size of this kid. no meds, no allergiesthat we're aware of. so where do you guys start? you arrive on scene. what are you going todo with that kid first? [inaudible] ok, so we just start withwe're walking in the room

and we do the across theroom assessment, right. as we're approachingthem, we're already trying to figureout what's going on. so when you're looking atthem, what are you looking for? is the breathing? yes, he's breathing. what's that? yeah, how mucheffort does he have? and he has, in his respiratoryeffort, he is breathing.

he has decent color. but he has forced breathingwith a longer expiratory phase than an inspiratory phase. what else do you want to know? mental status, he'snot responding to. longer expiratory thaninspiratory phase. what else would you like? color. color, pale to normalbut no cyanosis.

he has very poor skin turgor. blood sugar, ah, whata great question. blood sugar is 420. [laughter] all right, here's our vitals. so he's running 75 over 40. he's a six-year-old kid. do we know if that's goodfor a six-year-old kid? what's our pediatric formula?

anybody know this? so two times what? ok, so two timestheir age plus 70 is your baseline for thelower fifth percentile of where a pediatricblood pressure should be. so he's six years old. 2 times 6 is 12 plus 70. so he should be atleast 82, right? so how do we feel aboutthis blood pressure?

yeah, he's lower thanhe should be, ok. not critical, but he's lower. we've got pulse 150. for a six-year-old,where is that? it is too high. it is tachy. so he's showingsome tachycardia. respiratory rate, howdo you feel about that? so again, and we've got thatforced expiratory phase.

oh, what a great question. yes, it's very fruity,very fruity breath. what else wouldyou like to know? great question. there is grandmotheron mom's side and an uncle havediabetes type one. what other systems dohave in front of you that you want information on? yeah, mom has seen him goingin and out of the bathroom

quite frequently. so we can maybe makea presumption there. yes, he does. polydipsia, polyuria,and polyphagia. you asked about his skin, soit was poor, poor turgor, pale. he response to pain. so he's kind ofmoaning but really doesn't open hiseyes on command. so what do you guys suspect?

you've got a prettygood picture. ok, so it soundslike we've got likely the diabeticketoacidosis going on. what's happeningphysiologically in his system? ok, so what does ithave too much of? sugar. so it has too much sugar. and when you have tomu-- not enough insulin. so that's type onediabetes, correct?

so if you don'thave enough insulin, the sugar accumulates and weend up with these high sugars everywhere. so what does the bodyuse for an energy source if it can't utilizethe sugar that's got? ketones are the byproduct. right, so fat. so right, the body ismobilizing those fat stores. it's a very, let'ssee, ineffective.

it's energy inefficientto metabolize fat. so ketones are the byproductof the fat metabolism. but the body's trying toget energy from somewhere. and that's how it's generating. so with a byproductof ketones, what happens to theirmetabolic state? yes, too much acid. so we have those fatty acids. so they're acidotic.

is it a metabolicacidosis or respiratory? yeah, it's themetabolic acidosis. so what would weexpect if we, now do you guys have theability to do labs or blood gases on a rig? forgive me, because i'venot worked in your shoes. so i may haveparamedic questions. and you can educate me, justlike i'm sharing with you. all right, so oncewe get to the er,

if we're able to doblood gases, what would we anticipate those to be? what might that ph run? yeah, it's going to be low. so what's our normal ph range? 7.35 to 7.45. so it's not unusual for thesephs to be less than 7.3. very common to havethat derangement. what about bicarb?

what's the body doingwith the bicarb supply? yes, we are consumingit, because it's trying to balance out the acid. bicarb is a base. so they're reactingwith each other. and the bicarb storesare being used up. so all of thesequestions are important. because they're all going tolead to how we're going to take care of this kid.

all right, so here's a nicecomplicated little diagram about dka. whenever i see one ofthese in the textbook, let me share withyou how i start. because i'm also a student. i'm in my, i'm workingon my master's of science in nursing atalverno to be an np. so my pathophysiologybook has lots of these kinds of diagrams.

and the way i tacklethem is start at the top. you know, see whatwe're dealing with. so we're trying to chew ondka and what it's all about. and it's telling usthat we're trying to figure outmetabolically what's going on with that absoluteinsulin deficiency in that type one diabetic. then i'll look at the bottom. so the bottom is theoutcome that our patient

is experiencing. so diabetic coma, that'swhere this kid is at, right? and all of that junk inbetween on that complex chart, of course, thenhelps us break down what's going on system bysystem so we can understand that pathophysiologyof that disease. so we talked about the cellsare not able to use glucose. so we've got thisglucose usually over 300. that's kind of adiagnostic criteria

for type one diabetics and dka. if we were ableto do a urine dip, would we see a little bitof glucose in that urine? absolutely. we know about the polyuria. what signs do we have atthat the kid is dehydrated in our physical assessment? turgor. yup, blood pressure is low.

tachycardia. right, so heart rate's up. so we've got lotsof signs telling us that yes, he'sprobably dehydrated. he's been losing potassium andsodium as he pees it all out, all those electrolytes rightdown the toilet literally. so we've got low volume,increased heart rate, and then we talked about breakdownof body proteins, trying to get thatglucose level up.

we have the breakdownin the fatty tissue and the generationof the ketones. so here's the criteriafor diagnosing dka. we've got the blood glucoselevels by definition are greater than 250. the serum bicarb whenit's finally measured is going to be lessthan 15 does anyone know the normal rangefor sodium bicarb? 22 to 28, absolutely.

good job. ph is low, so we talkedabout that, less than 7.3. and ketonemia is theketones in the blood. so we will draw thatlab when they arrive, as well as get that urineand check for ketones there. so these are thediagnostics we'll use. so are our goals? this kid needs someiv fluids, yes. we need to improve his volume.

because he has beenlosing, losing, losing. and he's dry as a bone. so we want to get the volumeand get that tissue reperfused. we need to bringdown that glucose. but do we want to bringit down super fast? if we gave a wholeboatload of insulin and that blood sugarplummeted, what could we do? do you know the complication? this is where i like to draw.

i hope you guys don't mind. i like pictures. i'm very visual. all right. let me find a markerthat works better. all right, so if thisis intravascular, oh, i can't spell on the board here. and here's our extracellular,our extra outside compartment. when we have high bloodsugar, where's the glucose?

it's intravascular, right,it's outside the cell. so it would be a lotof glucose in here, so very highconcentration of glucose. so if you know the conceptsaround osmotic or oncotic pressure, when you have morelike a higher oncotic pressure or more solutes in one area,what happens to the water? right, it moves. it moves away. so if i give, ithink, oh, i'm going

to give a whole bunch insulin. and i'm going tolower this blood sugar and fix this kid, becausethat's the problem, right. now i'm going to take away awhole lot of this sugar that's flowing around. and where's thatwater going to go? it's going to go back. so initially it went out. now it's going to go back.

what if this is, what ifthese are brain cells? what if thesebrain cells are all of a sudden fillingwith a lot of fluid? because i loweredthe sugar too quick, the oncotic pressuredidn't balance out. right, so i'm going to endup with cerebral edema. so that's a critical thingthat we need to avoid. we're going to give fluids, butwe're going to give it at a-- we're going to giveit at a managed rate.

so initially, fora six-year-old kid, what's our formula forfluid resuscitation? 20 mls per kilogram, you got it. so we're going to start there,a couple of those boluses, reassess, and go from there. so they're going to get insulin. it'll be a low dose therapy. and they will likelyend up on an insulin drip in a pediatricicu eventually.

ideally. the good news is because thisdisorder is so well understood and so well studied, thatwhen treated properly, the mortality rate has reallycome down to less than 5%, as far as the epidemiology goes. questions? dka. we started with an obvious one. endocrine only getsmore complex after this.

all right, so dka goes tothe top of your column. let's begin case number two. all right, so another 911 call. we have the girlfriendcalling in this time, 56-year-old male patient. she says, my boyfriendisn't acting right. he's been sick for three days. now he's not making any sense atall as he tries to talk to her. she thinks something's wrong.

dispatcher gets afew more details. girlfriend says he's been kindof weak, just laying around on the couch forthe past three days. it's not like him. he usually goes to work. he is urinating a lot. and he's drinkinga lot, not beer. he's drinking lots of water. water and gatoradehe's been craving.

today she thinksbefore he became kind of this obtunded ornot responding to her well that he's seeing thingsthat aren't really there. he's talking a lot aboutsnakes on the walls. past medical history,she tells you that he is a diabetic type two. he's had this for 10 years. he's got a hypertension. oh, they don't checkblood sugars in the lab.

also a history of hypertension. he is quote unquote "dietcontrolled" for his diabetic. he also has a bmi, didi put that up here? no. he has a bmi of 42. so what's our normalbmi range that to be? 20 to 25 would be ideal. 25 to 30 bmi is overweight. over 30 is obese.

and then over 40is morbidly obese. so he's 42, bmi of 42. he's on metformin andhydrochlorothiazide usually. no allergies to medicine. so that's our initial call. all right, let'sbegin our assessment. what do you want to know? his mentation. ok, mentation is he'snot really talking.

you see a lot of twitchingall over his body. so you're on site now. you see a lot ofmuscle twitching, a lot of musclefasciculations going on. they really won't answeryour questions at all. what was that, rachel? ok, let's get some vitals. so we've got 95 over 40, pulse135, respiratory rate is 20. look at that temp.

he's 102.9. and pulse ox 97%. blood sugar you asked for, 850. yeah, how high doesyour monitor go? [interposing voices] 500, 600, yeah. i think ours in our lab,ours goes up to 500. so we'll get thisnumber definitively when we can send it tothe actual hospital lab.

it is a wee bit high. just for kicks and giggles,what is the normal blood sugar range? yeah, it's somewhere,i kind of, every book has a little bit ofa different range. and every lab hasa different range. so it's approximately 60 to100 or 105, somewhere in there. so yeah, this is alittle bit out of range. so yes, your monitorwould just read, high.

how long has he been sick for? ok, three days girlfriendsays, just feeling really weak. has called in sick to work. he is a construction worker. and he hasn't gone,hasn't gone to work. [inaudible] blood sugar. and he is urinating [inaudible]. ok, she wants toknow if there is a small, small,foul smelling urine.

there's a lot of urine. but there is nofoul smell to it. good question. breath sounds, he has normalrespiratory pattern and effort. respiratory rate 20. no increase work ofbreathing at all. he's on metformin. and the girlfriend tellsyou he hasn't had it filled for three weeks.

do you really want totake those work boots off? yes, he does smell like hehas some little pseudomonas in the feet going on. all right, so normalrespiratory pattern. we noticed the increase rate. it's a sinus tach. we've got him on the monitor. you could see that he's sinustachycardia, no arrhythmias. he's got the p's, polydipsia,polyurea, polyphagia,

according to the girlfriend. skin turgor is poor. we didn't ask that question,so showing signs of dehydration again. so he's aphasia currently. we see the muscle twitching. he's got the hyperthermia, whichcan be a neurological issue potentially, and thehallucinations as reported by our girlfriend.

all right, so iheard a suspicion. what do you think's going on? so hyperosmolar, hyperglycemic,nonketotic coma or syndrome, depending on whichtextbook you're reading. so sometimes it's hhs,sometimes it's hhnk. terminology varies. i agree with you. so what's the difference betweenthis disorder and diabetes type one with dka?

ok, so it happens tonon-insulin dependent peeps. he's got an underlying, or he'sgot a [inaudible] something else underlyinggoing on [inaudible]. yes, ok. so the wound connection, yep. we've got the lovelypseudomonas smell. he has a fever,[inaudible], something. so something is triggeringthis in his system. something is triggering.

what's the physiologicproblem with type 2 diabetics? do they make insulin? correct, yes. so the cells can't utilize theinsulin for whatever reason. he's making it. he's just not using it. so it's interesting,because they start to pour withthat polyuria, they start to pour theglucose into their urine.

so when we do thaturine dip finally, we'll see lots andlots of glucose. but as that sugar continuesto climb and climb and climb, then the kidneysstart to be affected. and they start to gointo acute renal failure. so now they can'tput out the glucose and it's just thisvicious cycle. that's why these sugarsare so much higher usually than the patients who are indka, because that vicious cycle

just keeps making itclimb and climb and climb. so hhnk, here'sanother lovely diagram. so you were right. environment, infection, oremotional stressors, something triggers this. and he's got thewounds on its feet. he needs to come seeme in the wound clinic. actually, he needs tosee me in the hospital. yes, so he's gotsignificant issues.

he has decreasedamount of insulin. so we have little breakdownof fat in the cells. the body ismetabolizing differently than it does in dka. so we don't havethe ketone bodies here that we wouldexpect in type one. the liver is breakingdown glycogen to glucose, leading to that hyperglycemia. so that's, again, one ofthose contributing factors

to that blood sugarthat's climbing so high. initially, you get the osmoticdiuresis through the polyuria until you end up withthe renal insufficiency and then the kidneys can'tput out the sugar anymore. they also end upwith hypokalemia. so he needs his potassium levelchecked, sooner than later. because as they are spillingout all of that sugar, with it goes quite a bitof the potassium. so they can end up shockyand in cardiac arrhythmias

as a result. so here's the definitivediagnostic criteria for the hhnk or hhs,blood glucose levels greater than 600. when they measure theplasma osmolarity, again what is that measuring? what does thatlab tests measure? concentration. yeah, yeah, you'reon the right track.

it's the concentration ofthe solutes in the blood, so proteins, anytype of molecule that has the ability toaffect where water goes, so that exerts an osmotic effecton cells or extracellular. hello. so plasma osmolarityis measured. and it's greaterthan 320, meaning he's got a whole lot ofstuff in there, in this case sugar, that's creatingthis dehydrating effect.

so pulls fluid again from thecells into the vascular system, and then the urinarysystem pees it out. so what's the stateof their general cells out in the periphery? if you touch test, ifyou test skin turgor, what's it going to feel like? yeah, very poor skinturgor, so again, they're going to be very, very dry. so we have no ketoacidosis.

so that's a majordifferentiating criteria. so the lack of the fruity breathwould be a key assessment. and the lack of thenormal respiratory status is a big clue, too, and thendepression of the sensorium. hallucinations are very common. so this guy is seeingsnakes on the walls, the electrolyte imbalance,and the hyperglycemia is causing more nervetransmission as a result. if you ask me to explainthe exact biochemistry,

i will not be able to. but it's a great question,all good questions. any other questionsor comments on him? no? ok. well, good jobwith the diagnosis. how are we going to treat him? we're going to, again, he needsvolume, just like the kid did. so we need to improvevolume and tissue perfusion.

we need to bringthat glucose down. we need to fix the potassium. very, very careful,you know, he probably bought himself an admission toan icu bed in most facilities. and then cerebral edema here canbe another major complication of rehydration. so low, slow and low,leveling or correction of that blood sugar. so we're going to do low dosetherapy again, iv fluids.

and this one does havea much higher mortality, especially when you thinkabout that there's usually an underlying causethat's triggering this. so he's got this infectionhe's dealing with, wounds that won't heal. his body's in a worldof hurt right now. usually, like ourpractice in the er, what i would usuallysee the er providers do is order somewherelike an 8 to 10

unit regular, unitsof regular insulin. and then we wouldstart the insulin drip, again at a lower rate. and then they get q1 hourglucose checks with, you know, you're talking to the provider. how do you want thisadjusted based on, so it's a verycontrolled lowering. it is going to take a long time. but the goal is not tocause this cerebral edema.

so we do want it to lower. the body has adapted over time. because he hasn't had hisdrugs for three weeks. you know, this sugar'sbeen climbing and climbing and climbing for muchmore than three days. he's only felt sickfor three days. so we have to bring itdown low, low and slow so, so the body can adapt. his therapy in the er,what i would anticipate

would be the insulinas we discussed. he's going to get iv fluids thatare going to have a potassium supplementation tothem, so it's going to be like a normalsaline with 20 of kcl added in his liter bagat a controlled rate. he is going to get,the doc's going to see right away thatlovely pseudomonas. so we're going to start,we're going to get cultures, blood cultures.

and we're going to getiv antibiotics on board. those antibiotics are not goingto affect his insulin drip treatment? it shouldn't. probably he'll end upwith different ivs. so he'll have to have two ivsites dedicated for an insulin. and i had interestingexperience at waukesha. i had the opportunity to bepart of a root cause analysis. are you guys familiar withthat term, root cause analysis?

so something goes wrong. and you come togetheras a team to try and figure out whatprocess went wrong and why the patient didn'tget the ideal treatment. so it was a dkapatient that ended up on an insulin drip thatwas sent to the icu. and do you guys usepumps in your rigs, or is everything open? you have a pump?

ok, so there are somepumps, some are free hang. ok, so pumps are really a giftto bedside care providers, you know, because theyallow us a lot of control. but they also can causeproblems if not used properly. so what happened with this dkapatient is the insulin drip was mixed, primed, and hungas a secondary infusion. so you've got your primarybag plugged into the pump with a rate, sayit's a rate of 100. then the staff hung theinsulin as a piggy back

into that, programedit to do so many units for a certain period of time. and when that time was up, itswitched back over to primary. the patient went withouttheir insulin for six hours before it was discovered. so safety if running aninsulin drip, what we learned and how the policywas changed, that it needs to be on a primary line. it can never be asecondary infusion.

and you know, itmight not have, you know until somethinglike that happens, you might not even think aboutit to that level of detail. so the patient was fine, fine. they corrected it. but you know, it'sagain six hours that they needed insulinthat they didn't get it. all right, so i just pulledthis table out of one of our pathophysiology booksreally to kind of compare

the two, just to showthose differences, reiterate betweenthe dka and then the hyperosmolarity,nonketotic, hyperglycemia. so you can see thatthe nkh or the nnk, however you want to, hhs,whatever you want to call it, glucose much higherthan the glucose in dka. you can see it's type oneversus type two usually. dka has thatprecipitating event. fluid losses, thisparticular book

addressed the fluid losses. you can see how muchfluid the body does lose. the hhnk tends to be adryer patient than the dka. clinical presentation,our little kiddo had all of those symptoms. the older adult wascertainly approaching that with his aphasia andhis neurological status. higher mortality ratereported in this source. treatment, insulin,saline, potassium.

and then complications,we all discussed. so just kind of a nice side byside showing the differences. all right, ready for case three? all right, you're sittingin a classroom listening to an absolutely rivetingtalk on endocrine emergencies. you hear a thud in anearby seat and see a classmate slumpedover a table. before coming to the conclusionthat he is just bored and or tired, you alsonotice that is profusely

diaphoretic to yourtouch and clammy. so where are we going to start? call 911. excellent, let's call for help. because we don'thave, i don't know if we want to trust any of theresources in the room here. they're educationresources for a reason. are they breathingor [inaudible]? ok, yes, they are breathing.

do we-- what's their rate? what's their breathing rate? their respiratory rate is 26. no, i'm sorry, 18. 18. so of course it's a friend, it'sa colleague in the classroom. we don't know jack diddlyabout their background, right. so we don't knowpast medical history.

we don't know meds. we don't know allergies. we dial 911. you guys did that. very limited resourceswe have available. yeah, exactly. so we have to completely rely onour physical assessment skills, right? so let's physicallyassess them while we're

waiting for our 911compatriots to arrive. oh, it's bouncing. look at that. all right, so we grab a bloodpressure cuff from the room. we get 120 over 75. someone's palpating his pulse. and we feel it coming about 125. respiratory rate is 18. temperature 97.9, andwe used the red probe,

just for the record, ok. and pulse oximetry, 98%. so any concerns inthe immediate vitals? ok, so he's got the tachycardia. but everythingelse is pretty ok. all right, so what elsedo we want to look at? are they [inaudible]? aha, blood sugar. so we pull out our handy dandypractice blood sugar machine.

and we get 26. oh. so was this person likehaving all this [inaudible]. they came in late with acup of coffee in their hand. he was complaining, youheard him complaining about how hungry he was becausehe had to skip breakfast. he does respond painful stimuli. [inaudible] i mean, for-- diaphoretic, skinturgor is normal.

he has a bracelet that's sayshe is a type two diabetic. you know, hypoglycemia. all right, so we'vegot hypoglycemia. all right, so by definition,it's a glucose less than 60. but people startto have symptoms at all different ranges, right? everybody is veryunique, very unique. when i had a caseof radiology, we were doing an angiogram onan older gentleman's leg.

we finished theangiogram, move him from the procedure tableback to the stretcher, and all of a sudden, heslumped over with a facial drooling and notresponding to us. well, we're in radiology. what do we automaticallystart to think? stroke. stroke, and where do we go,because we're in radiology? straight to ct, right?

we're going to belike super ct people. [inaudible] blood sugar? we did. until he was halfwaythrough his ct. and it was 27. we just spent $4,000to fix a $0.50 problem. so yes, blood sugarcrucial, crucial to check. all right, so treatment options. these are thegeneral guidelines.

again, it's going to varyby protocol by patho book. our goal is ifthey're awake, what's your criteria forgiving oral glucose? ok, all right. so is he doing that toowhile slumped over the table? all right, so we have toskip the 50 to 20 grams of oral glucose in thisparticular individual. glucagon im. intranasal?

if you've got thatoption, that's fantastic. so that's an optionif we've got that. or if we start that iv,we're going to do that bolus. and when i startednursing back in '99. '99 was my graduation date. so initially, we would alwayspush that entire amp of d50. now they're gettinga little bit more selective with howmuch we start with. have you guys seen that, too?

yeah, give a half amp instead. because we're causingthem to rebound so far in the other direction. we're forcing hyperglycemiaon them, which is also good. so the range is 20 to 50milliliters of that 50%, that d5 dump. all right, so our classmatewakes up, gets his sugar. and you learn that he's anewly diagnosed type two diabetic with a recent changein diabetic medications.

so they've been monkeyingaround, trying to get them. he's running late thismorning and consumed nothing besidestwo cups of coffee. but he did take his meds. so here we had alittle bottoming out, some hypoglycemia. in doing the reviewfor this class, when i was readingabout hypoglycemia, there are people,now have you known

people who can feel whenthey're getting low blood sugar? there are people thatcannot detect it. so they might bedropping 60, 50, 40. and they have absolutelyno indication symptom-wise that they're droppinguntil they pass out. so it's just socrucial to remember everybody is such adifferent individual when we're dealing with this. questions on hypoglycemia?

all right, casefour, all right, we have 35-year-oldfemale discharged from the hospital two days ago. she had neurosurgery. they took out a benign growthfrom her posterior pituitary gland. she has called 911 becauseshe is profoundly weak. and she's havingprofuse urination. i just can't stoppeeing and drinking.

i have no one at home tobring me to the hospital. help me, is what she says. ok, so you'redispatched to her home. you find no otherpast medical history, other than thisbenign tumor that was, she says it was found asan incidental finding on ct after she had a bicyclecrash and she hit her head. so they did a ctas a precaution. and they found this tumor.

no meds, no allergies currently,other than some pain medication maybe for headache. so where are we going? she was diagnosed with aconcussion, no bleed, no bleed. they just said, take it easy. you have concussive syndrome. she was told thatit might last, she might have some symptomsfor three to six months, but no long termeffects expected.

all right, so what else dowe want to do in the home right there? what other informationcan we gather? ok, good, all right sovitals, 110 over 65, pulse 98, respiratoryrate 16, temperature 98.9, pulse oximetry 98%. how do you like those vitals? i'm pretty cool with them. i thin they're good.

all right, what elseshould we check? what could we do rightthere in her home before we transport her? blood sugar, 95. nothing jumpingout at us just yet. ok, let's get a 12 lead,normal sinus rhythm. respiratory youcan see up there. yeah. and the pituitary.

yes, there issomething going on. is it pete? no, paul, sorry. had to peek. paul's on the right track. he asked aboutvasopressin, vasopressin. something, what's theother name for vasopressin? antidiuretic hormone, yes. so in someone whose pituitaryis functioning normally,

what does antidiuretichormone do for us? right, so if youhave a normal amount, yes, so the higher it is, themore water retention you have. so if it goes the otherdirection, what happens? all right, so nowyou're going start, if you don't have any tohold the water in your body, now you start emptying itout, so which way is she going does it sound like? ok, so probably low.

so your anticipation thatshe has a low adh level is right on target. so that gi/gu system,we know she's polyuric. she's also beenprofoundly thirsty, trying to keep up with it. she's going to the bathroomevery 10 to 20 minutes, drinking water constantly. otherwise no othergi/gu symptoms. what else are we assessing?

skin, ok, skin turgor warm anddry at this time, could change. neuro status, she's appropriate,totally appropriate. answered all questionsappropriately, so essentially withinnormal limits. a little fatigued. all right, so whatdo you guys suspect? so we talked aboutadh, too low of an adh. what there is a conditionthat causes too low of adh. does anybody remember thename of the condition?

i hate the name of it,because i always confuse it with the first threethat we've already about. here's a clue. ok, so here again,just a diagram looking at the pituitary gland. so we've got theposterior pituitary that puts out the adh. it's also responsible forother hormones as well. but we've got that failureof that water re-absorption.

ok, there it is. there it is. diabetes insipidus. that's why it's so confusing,because when you hear diabetes, what do you think? sugar, sugar, sugar, right? i have not come across amedical emergency related to too much or toolittle oxytocin. so that's out of my scopeof knowledge, to be honest.

yeah, yeah, i thinkyou have to spelunk into some deep gyn or endocrinetexts to find more about that. but it is a reasonable question. so diabetes insipidusis not about sugar. it's all about the adh. so this is one ofthose little things that you've got topound into your head. so we have a deficiency ordecreased response to adh. look at that liters ofurine daily, three to 20.

that is a lot of fluid. you are peeing your mind out. there goes your quality of life. you're in thebathroom all the time. lots and lots ofthirst, now she's been able to keep upfor the most part. if you are able to take in asmuch as you're putting out, there will be verylittle symptoms, as evidenced byher vitals, right?

she's not tachy. skin turgor's ok right now. she seems to be compensatingwith her drinking. if the patient thenbecomes compromised, let's say that they're notable to take in fluids, this is where we startto get in trouble. because now they're going toget that profound dehydration. because they're not takingin what they need to. so how do they diagnose it?

unfortunately, can't justmeasure a plain old vasopressin or adh level. that lab test doesn't exist. so the diagnosticprocess for this is they're going to have a 24hour urine measurement looking for, what's the hormone thatstimulates the pituitary gland? where does it come from? yeah, it comes fromthe hypothalamus. so we're looking atadrenocorticotropin, acth

hormone. so they're going todo some acth levels, looking at the output ofthe hormone over a 24 hour period of time in the urine. we also need to make surethat we don't have the glucose issues, so they're going todo glucose studies as well, make sure that there's noother signs of diabetes. they need to checkfor renal dysfunction. and treatment for thisis very conservative.

so again, they're going tolook at that cause as to why, you know. we kind of know why, right? her posteriorpituitary was recently impacted by thetrauma of surgery. they're going towatch her over time. the ddavp is a substitutevasopressin drug that can be given. but it's not a firstline treatment.

they're going to evaluate. they're going to doall the diagnostics, make sure that the fluid balanceis obtained, and go from there. all right, fourmore case studies will get us throughthe endocrine. flipping to the back side. before we jump into some ofthese other unusual conditions, i just wanted to take a momentto talk about the hpa axis. what the heck is the hpa axis?

so this is thehypothalamus-pituitary axis. you know that our hormonesare all on a feedback cycle, right, from somewhere alongthe way in your studies? so if we're talkingabout thyroid, the thyroid is going to producea certain amount of hormone until we've reachthe desired level. then the hypothalamus says, eh. pfft. you're good.

knock it off. we don't need anymore right now. so it's a really nice feedbackloop that most hormones run on. and they're allcontrolled, these are controlled by the hpa axis,so hypothalamus-pituitary axis. so they start with, you've gotthe releasing hormones, so up here at this level,thyroid releasing hormone. i'm blanking now on whatthe crh, the c stands for. something releasing hormone,cortisol releasing hormone?

corticotropin. sorry. then these othertwo are important, but don't necessarilydrive endocrine emergency. so it's the first two we'regoing to specifically focus on. because that'swhere we might find these patients in dire straits. so thyroid releasinghormone comes out of the hypothalamus, actson the thyroid itself.

so you've got the tsh hormonethat comes down, knocks on the thyroid's door,says get to work buddy. we need you to producesome t3 and t4. so that's our endproduct, is our t3, t4. likewise for theadrenal glands, we've got the acth that is secretedthat acts on the adrenals and tells the adrenalsto pick up production. again all, oncethey're circulating, the hypothalamus should get themessage and cut off production.

when that doesn'thappen, that's when our patients run intoa lot of problems. so here's the defect. they can be classified. again you don't haveto, i don't think, differentiate at this level. but we'll touch on it justto kind of paint the picture. a primary problem is going to bean abnormality in the gland, so hashimoto's thyroiditis.

the gland has been destroyedby an autoimmune disease. and it can no longerproduce t3, t4. or it produces too much. secondary, that wouldbe the pituitary gland that's malfunctioning. so it's getting,it's got a tumor, or it's got something going on. and it's sendingout errand signals. and it's not respondingto the pathway.

and then the tertiary level iswhen the hypothalamus itself, so the ultimate controlmechanism is going high wire. so it's either sendingup too much stimulation or not enough and notresponding to the feedback loop. so case number five, wehave 45-year-old female who calls for help complainingof nausea, vomiting, my favorite er chiefcomplaint, weak and dizzy. everybody's weak and dizzy. especially withposition changes,

really dizzy when shegets up from sitting to standing, or fromlying down to standing up. she tell you she has ahistory of addison's disease. and she's recently been treatedfor bronchitis, last 2 and 1/2 weeks or so, prettyprofound cough. she's on hydrocortisone. why does she take that? ok, so let's talkabout addison's. what does it mean when youhave addison's disease?

say again. that is we have, it's the othergland we're talking about, adrenal gland. so addison's isrelated to adrenals. that's another one. you don't produce thecortisol you need to. yes. [inaudible]. right, so your medicationhere is your clue. so this is her replacementhormone that she's taking.

so she doesn't haveenough cortisol. so she's on hydrocortisoneas her daily med. addison's diseaseagain believed to be another autoimmune disorder thatdestroys the adrenal gland's ability do its job. so now it cannot secrete, eventhough it might be getting the messages. so if you were tosee some past blood work in her diagnosticprocess for being diagnosed

with addison's disease,which one of these would you expect to measure? and what would the result be? acth. why would it be low? if you have not enoughcortisol, what's the hypothalamus going to do? it's going to increasethe acth to try and get the adrenal glandsto do their job.

[inaudible] elevated. so your acth levels willbe through the roof, because the adrenal glandscan't respond to them. hypothalamus is sendingout the messages but adrenals aren'tgetting them. so in her processof diagnosing, she had acth levelsthat were too low. and they studiedher cortisol levels. and she had little to none.

she's allergic to penicillin. just had to throw anallergy in there somewhere. all right, sophysically, what do we want to check her out for? what are we looking at? mhm. i know what you're getting at. orthostatic blood pressure. orthostatic blood pressure, ok.

so let's get some vitals. initial bloodpressure, 70 over 45. this is laying down. you want to stand her up? all right, we'll start there. all right, pulserate, a little fast. she's at 132, respiratory rate24, temperature 95.9, pulse oximetry 97%. she is.

she is answering questions. seems appropriate, other thanjust being very weak and tired. i would do a blood sugar on her. blood sugar's 54. skin turgor is, herskin turgor is normal. but as you arelooking at her skin, you noticehyperpigmentation, especially in all of her skin creases. it is.

why is it, any ideawhy it's normal? it's one of those triviaquestion about addison's. it's not something onthe test kind of thing. the acth that thehypothalamus is pumping out trying to get theadrenals to respond is very close to the hormonethat stimulates melanocytes that causes the developmentof skin color, color. so you have all thisextra acth in your body and it gives the skinthis different color

to it, especiallyin the creases. it really, you'll seethat darker coloration that you wouldn'tsee in a normal. usually we're palerin those areas, so you would see thedarker, darker coloration. she has cramping inher muscles, kind of some leg cramping, somehip cramping she's feeling. not a real specificpinpoint area, just generalized cramping.

all right, let's get a 12 lead. she has a sinus tachycardiawith peaked t-waves. what causes peaked t-waves? yeah, she's gottoo much potassium, too much potassium, all right. respiratory'sslightly tachypneic. she still has that residualcough from the bronchitis probably. she's still workingon her antibiotics.

she complains of some nausea,vomiting, very poor appetite. you notice thehyperpigmentation on the skin. neuro, and then justoverall general very thin and bony, not goodmuscle tone, just doesn't look like she'swell nourished at all. skin and bones. so somebody her age,very unexpected. all right, so what do wethink's going on right now? she has a history of addison's.

she has a recent infection. will that exacerbatethose symptoms? yeah, it will. it will. so you've gotaddison's, where you have the lack of the hormone. and you're replacingit with hydrocortisone. so what happens when theinfection triggers her system? yeah, it's not enough, right.

she's not getting enough. because what iscortisone known for? what kind of hormone? stress. stress, it's a stress hormone. so her body's stressedby the infection. the baseline hydrocortisonedosing that she's got is not enough to gether body through this. so what's the conditionthat she's in?

what would be theemergency condition that we're finding her in? it is a crisis. it's acute adrenal crisis. so she has way, way too littlehormones coming from that glad. the hydrocortisone is notenough to get her through. so she is in a lifethreatening situation. we cannot survive withoutour adrenal hormones. we've got cortex hormones.

we've got medullary hormones. where doesepinephrine come from? yeah, yeah. so it epi is an adrenal hormone. we've got then ourmineralocorticoids, our glucocorticoids,all part of metabolism. why do you thinkshe's so cachectic? she can't, you know,she's not metabolizing. she's not utilizing energy wellin her body to build muscle.

why would she be hyperthermic? what would makeher hyperthermic? you're saying it's not burningthe energy to create the heat? or it is burningenergy to create heat? it's trying to, but it's not. she's really thin, reallythin, so doesn't really have the ability tomaintain body temperature. she is frail. for being a youngas she is, she just

doesn't have the fortitude. the condition itselfdoesn't necessarily cause hypothermia,or hyperthermia. it did, when wesaw, which condition did our guy have areally high temp? the hhnk or hhs, yes. that one is very muchassociated with hyperthermia, with or without infection. you can just havean elevated temp.

this one wasn't somuch saying that that was a primary symptom. all right, so commonpresentations, looks like she's got them. you know her, what wasthat blood pressure we had? it wasn't too good. so she's kind of on thatroad to vascular collapse. we need to dosomething about that. so for acute adrenalcrisis, there's

five s's for management. they have been losingsalt and sugar, so they're going to getan iv maintenance drip. it's usually goingto be normal saline with d5 added, 5% dextrose. they need moresteroid replacement, because her hydrocortisoneis not doing the job, right? dexamethasone is likelygoing to be our choice. it's going to act forabout 12 to 24 hours.

and it has a littlebit more potency than the plain hydrocortisonefor getting on board quickly and doing an effective job. so neither one isfine, but dexamethasone is the preferred steroid. it's going to be a push. it'll be a push drugthat they'll get. it does take about five tosix hours for it to kick in, steroids, of course,are not fast.

but so we'll have to dosupport, physiologic support, in the meantime. so she will likely end up inthe icu for ongoing monitoring management. and then search for andtreat that underlying cause, because something,like we talked about, something triggered it. so she had bronchitis. maybe it was limitedto bronchitis,

but maybe what mightit have progressed to? pneumonia, so we're goingto get a chest x-ray. we might anticipatesome treatment in that regard for her. continuing on this pathway,next call comes in. the husband of a64-year-old female calls 911 to report thathis wife slipped on a rug and fell to the floor. she now has excruciatingpain in her upper mid back.

he can't get her off the floor. any time he touches her,she just screams in pain. so he's calling for helpto get her up off the floor and fix her, of course. he denies that shehas any known history. however, you findout that she really hasn't seen a doctorin over 30 years. she is a hot mes. you look at her, andyou're like, oh, honey.

you've got diagnoses. we just don't knowwhat they are yet. yes. all right, so deniesany allergies to meds. she's not anymedications, of course. so physically,let's start there. did she hit her noggin? [chuckle] what a great question.

and she did notlose consciousness. and she did not hit her head. slipped on a rug, fell. orientation, she iswithin normal limits. what she doing? she was reaching for something,lost her, kind of slipped on the rug as she wasreaching and went down. did she requireassistance at all? not before, notbefore this fall.

she does remember it. did she feel funny before it? she says that she has,let's see, she's fine. i'm fine. leave me alone. [laughter] whatwas your question? any obvious injuries? when you palpateher upper thorax where she's complainingof pain, she

has pinpoint tendernessat t11 and t12. low blood sugar. maybe that's why she fell. blood sugar is 256. ok, vitals 165 over 105, pulse110, respiratory rate 26, temp 95.9, pulse oximetry, 97%. drinking? she says that she has two drinksevery night, two high balls. what did you say, rachel?

stroke scale. stroke scale, she is, let's see. she is a, which strokescale are you using? normal, then normal limits. what about [inaudible]? i'm like, well, i'm justgoing to whip out an nih. i'm like well, we know don'tusually use that pre-- yeah, we don't even usethat in most ers. no neuro deficits.

no neuro deficits at all. she's a little, she'sa little emotional. she's a little cranky. she doesn't want togo to the hospital. but she can't get offthe floor on her own because of the intensepain in her upper back. no, no back painbefore the fall. exactly, so we're going toschmooze her to the hospital, schmooze her in for evaluation.

all right, what othersystems can we assess? ok, so let's get a 12 lead. qrs complex is amplifiedand slightly widened. we have normal respiratorypattern and effort. on both sides? both sides. she just doesn'twant to take breaths because it hurts in her back. and there's nothing,no bruises on the back

that we can see or feel? no, it's pinpoint, it's pointtenderness to the cervical, or the thoracicvertebrates themselves. what do you thinkis going on there? what kind of fractures? this fracture is significantto this condition. any fracture, anybone fracture, is significant to this condition? yes, she has osteoporosis-typetype symptoms that have let,

you know, she justslipped and fell. but now she's got this crazytenderness in her back, doesn't even have to beprecipitated by trauma. so she has compressionfractures back there. well, she is-- she has osteoporosis, so she'sbeen leaching calcium out of her bones, because she'sgot some kind of imbalance going on. it's an endocrine lecture.

of course she has animbalance going on. we've just got to get to, we'vegot to get more of the details. the cardiac stuffis significant, even though it's not like blah. any idea why you might have anamplified qrs complex, slightly widened? what is the heart muscle doing? don't think electrolytes. just think about isit easy or tough?

which condition has a reallylow amplitude, lower amplitude? think trauma. tamponade. so why is the amplitudedecreased in tamponade? it's constricted. but it's also,remember we have leads on the outside of the body. and it has to travel-- yes, it has more stuffto travel through.

so here we have thisparticular amplitude is related to increasedin the left ventricle. so she has left ventricularhypertrophy related to her disorder. so you're seeing thesesubtle signs on this 12 lead, because there'smore muscle there. so you're getting a greateramplitude of electricity through that heart,if that makes sense. specifically diagnosed, likeif you're getting into your ecg

definitions, if you'relooking in lead avl, it has to be greater than 12millimeters tall to actually be diagnostic for leftventricular hypertrophy. another thing that she tellsyou when you ask her about gi stuff she's been havingsome black stools. oh, you know, normal stuff. you know, they eat a lot of fastfood, and-- what that's that? tarry? yeah, they're black.

they're tarry, black stools. they've been going onfor about two days. she says it happens off and on. again, never seena doctor for it. skin tells us a fair amount,too, about these conditions. so when you're lookingat her skin condition, very parchmentpaper-like, so very thin. you can almost see through it. you also noticeprominent facial hair.

she's got a stash and a beard. bingo. because she hascushing syndrome. is that what gaveit away, the hair? and of course, if this ladywas right in front of you, you would noticethis right away. i mean, you couldn't miss this. the other thing thatshe would have would be, what would her body type be?

yeah, yeah, in thebelly right, right. so neuro, she'smentally appropriate but she's got that weakness. we've got the pointtenderness we talked about. and then here are thoseother characteristics. buffalo hump, whenyou actually lifted up her shirt to do her ecg, yousee these big, bright purple striae, stretch marks. the excess hormone causesthe skin to weaken.

so you end up withthese stretch marks. so yeah, she's gotthe thin extremities. so she's got like the bird-likelegs, the bird-like arms, but all the mass iscentered, central mass. a few peeps like that? all right, so cushing's. roz nailed it on the head there. so cushing can be caused byseveral different conditions. again, we're not going toknow until we get her there

for further diagnostics whatthe underlying issue is. but it could be thatcrazy pituitary. we've got a tumor in thepituitary secreting acth like crazy. and because theadrenals are fine, the adrenals can pumpout the cortisol. so we got crazyamounts of cortisol. why is her blood sugar high? cortisol, it stimulatesthat whole process.

we might have adrenalcushing syndrome. well, let's go back to this one. so pituitary cushing,where are the acth levels? high, low, or normal? it's a pituitary tumor. where does acth come from? so it acts on the adrenal. it acts on the adrenal. so if the pituitary isspitting all this out,

so the hypothalamustalks to the pituitary, which talks to the adrenals. so the pituitary isspitting out the acth that talks to the adrenals. so the tumor isin the pituitary. and it's producing lots of acth. so your acth levelis going to be high. and your cortisol is high. because the adrenalscan respond.

now if we have a tumorin a different location, so the tumor is nowin the adrenal gland, where's the acth levelfor the pituitary going to be when measured? it's quite low, right? because the feedbackmechanism is working. the cortisol is reallyhigh, so the hypothalamus is not going to communicateto the pituitary at all. it's going to keep the acth low.

but you've got this rogue tumorin the adrenal gland that's just pumping it out. so cortisol is high. small cell lung cancers,the number one culprit of these paraneoplastictumors that secrete hormones. so if you find out someone isbeing treated for small cell lung cancer, the nextquestion is, you know, have you ever been told thatyour tumor secretes hormones? because it might becoming from this external,

so if there's nothingwrong with the hypothalamus and the pituitary gland, butit's the lung or the tumor, wherever it is, that'sputting out acth. and then can people take drugsthat cause cushing syndrome? what if grandma took her wholebottle of hydrocortisone today? she's an addison's patient,but she took the whole thing because is a little demented,a little demented this morning. so you can certainly induceit by orally consuming. or if someone takes an overdose,they could have it as a result.

so you're not going to see thelong term changes over the body like we see in ourlady here, but we would see these type of symptomswith the sugar and the vitals. here's pictures ofsome of those folks, so you can see again,the female front and and in center thatshe's got the hirsutism. so you've got the hair onthe stash and the beard area, moon face, very easily bruising. that's a great pictureof stretch marks.

i mean oh, they're soprevalent, much more than from childbirth ornormal weight gain. you can see the central obesity,the stick legs, stick arms, holding all that weight central. so the picture on theright of that slide again just gives you kindof a whole list right out of the book of all of thosedifferent components of cushing syndrome. so diagnosis again,in the hospital,

she's going to get that 24hour measurement of cortisol. they're going to watch forpatterns, because again, cortisol is a verycyclical hormone. different times of the day,we secrete more than others. that's why they need a 24 hourmeasurement get an overall look at total secretion. they're going to look atthe plasma acth levels. and that'll help us figure outwhere this extra secretion is coming from, whether itbe pituitary, adrenal,

or a ectopic, and thenif appropriate, you know, tumor screening viamri or ct, if they're able to narrow it downto a suspected tumor. so our goal, removeor correct that source of hypercortisolism. it's probably notsomething we're going to do pre-hospitalor in the er. so we're going to supporther, getting her there. can we treat her pain forher compression fracture?

that's probably avery nice thing to do. maybe she'll end up inthree or four weeks coming to see us in interventionalradiology for a little kypho or vertebroplasty, ifthat's appropriate. but they may heal on their own. as far as the hypercortisolism,they have to decide. you know, is this a tumor thatcan be removed surgically? is it cancer that needs to betreated with radiation, say if it's the lung cancer?

or are we going to treat withsomething that blocks cortisol? those three drugs, mitotane,ketoconazole, and metyrapone, did i say that correctly? those all block theactions of cortisol. so those might betreatment as well. again, i've never seenthem given in the emergency department environment. it's usually somethingthat comes down the road from a specialist.

they get a little harderas we go along don't they? all right, so thisis another weird one. we don't see this very often. again, all right,72-year-old female collapses on the floorof her living room. husband is unable to wake her. he dials 911. and you're dispatchedto the house of this unresponsive woman.

she has a history ofhashimoto's thyroiditis. what's the pathology? what has the body, whathas her body done to her? something with the thyroid. thyroiditis gives us a clue. it is autoimmune. so her immune system hasdone what to her thyroid? it has destroyed it. it has destroyed it,absolutely destroyed it.

so it's an autoimmunedisorder, takes out the thyroid completely. so what's the treatment? so what's on her medication? levothyroxine. so if she's gotsynthroid, levothyroxine, she's got a replacementthyroid hormone. because her thyroidcannot produce. does her hypothalamus work?

does her pituitary work? yep. but her thyroid doesn't. so which hormone isgoing to be elevated? which measurementwill be elevated? what stimulates? thyroid [inaudible]. yep, so the trh fromthe hypothalamus, the tsh, thyroid stimulatinghormone, from the pituitary

are going to be way up. because they're going tobe trying to stimulate that thyroid to work. but the thyroid iscompletely out of business. they have a close signon the front door. and it's not doing anythingat all so that's her history. all right, so well, whatare we going to check? start with our assessment. blood pressure.

blood pressure, oh, crap. checked it three times, this isall i'm getting for you, 65/30. pulse rate 50. seven. respiratory rate is seven. if it's less than eight,we need to intubate. somebody taught me thatsilly phrase somewhere. all right, temperature. we got a problem withthat temperature?

91.9. if i get that with thetympanic temperature, what would i need torecheck that with? let's get a central temperature. yeah, let's getout that red probe. pulse oximetry is only 86%. well, she's only breathingseven times per minute, so some hypoxia going on there. so not a great setof vital signs.

she's got a lotof issues, right? all right, let's keepgoing on our systems. what are you checking next? 12 lead. 12 lead? blood sugar. blood sugar's 48. respiratory, obviously you knowshe's got a slow heart rate. you see circumoralcyanosis around her lips.

ok, drop an oral and bag her. so we recognize anairway issue right away. and we're going to address it. awesome. she's bradycardic. husband says she hasn't beeneating well for the past week. she has history ofdiminished perspiration. she doesn't make a lot of sweat. does not tolerate the cold.

skin is very pale. you notice she haslittle to no eyebrows. only the littlecenter bit is left when you're looking at her face. she has very coarse,dry, and brittle hair. husband said she's been verylethargic, very forgetful recently, just overall veryweak, which is unusual for her, he said. so what's going on?

so we know she's hypothyroidfrom the hashimoto's and takes the replacement. but what's go, is she even more? like right now, for somereason, she is having problems. because the thyroid, again,whatever she's getting isn't enough for hercurrent situation. she's a bigger lady. bmi is 32, so she'snot wasting away. you could, yeah, if she hadstopped her levothyroxine

all of sudden, cold turkey. you need it to live. so there is a condition. there's a name for this. she's not responding,so it's a coma. do you know the first word? it's a weird little word. myxedema, myxedematous coma. so the skin changes.

they have a very, itgets that term, myxedema, from the skin changes. it's a very waxyappearance and feel to it, almost like you'reat madame tussauds and you're feeling a wax person. so that's that kind ofthat meaning of myxedema. so she's certainly inthat comatose type state. so this is a life threatening,end stage expression of hypothyroidism.

could be from lackof medication. could be somethingthat has triggered her. she's no longer respondingto the thyroid hormone. what we'll see when westart to look at her labs is that her respiratoryrate is depressed, so she's now retainingcarbon dioxide. she's got that slow respiratoryrate, the low oxygen level. she's going to have significantfluid and electrolyte imbalances and hypothermia.

this is a veryclassic presentation of end stage hypothyroid. so how are we goingto save her life? all right, soaggressive management. she's full code, sowe'll get her intubated. we're going to warm her up. we're going to do--the warming piece is kind of a little asterisk. we need to do that slowly.

because if we warmher up quickly and we dilate all ofher blood vessels, where's her bloodpressure right now? in the tank. and if we dilate allof her capillary beds by warming her up just likethat, where's her fluid going? periphery. we're still not going tohave a blood pressure. so rewarming is slow.

she's going to needsaline running. because she's goingto, hyponatremia is classic with this. and we need to get thosethyroid hormones back on board. we find out that she's beentaking her vitamins instead of her thyroid meds. she has what seems to bea little bit potentially some undiagnoseddementia starting. so husband gets the pill bottle.

and we count the pills. and there's too many forwhen they were filled. all right, so she'soff to the icu as well. all right, last endocrine case. another 911 call, 30-year-oldfemale calls for help, complaining of palpitations,fever, shortness of breath. she recently hadwhat she thought was an upperrespiratory infection. but she woke up todayfeeling deathly ill.

how's that for vague? nice and vague. pretty common. she denies any pastmedical history. but she doesn't see aphysician for routine care. she's 30. i don't need to see a doctor. i just go to planned parenthood. i get my pills.

you know, i'm on birth control. and they do my female exam everynow and then, she says, too. so she's on birth control, noallergies that she's aware of. so let's jump in. get the set of vital signs. she's 95 over 70. according to aclsguidelines, we're ok, right? we're above 90, butstill very borderline. look at that pulse.

ok, so she's clipping along. she said she'sfeeling palpitations. now we got thistachycardia as well. respiratory rate,we're up there. look at that temp, 103.9. is that a normalinfection related temp? not usually, yeah. so we start to think about othercauses when it gets this high. and she's pretty youngto have a pulse ox of 92.

she's a non-smoker. not too happy with that. all right, we check her sugar. it's 105. and title co2. i don't have, she'snot intubated. all right, sorespiratory assessment. she's short of breath. and you auscultateand she has crackles

from the mid to the bases. and she's a nonsmoker. cardiovascular, wesee the tachycardia. and she says she's beenhaving palpitations on and off for a couple of weeks,much more frequent in the last three days. she says she has atremendous appetite, just can't get enough food. but she keeps losing weight.

no, it hasn't. this has kind of ramped up. this is the firsttime ramping up. she tells you she's lost50 pounds in the last seven months. all right, so in thatintegumentary system, she's got excessive sweating,can't stand the heat at all. she just wants golive in alaska lately. hair is really thinand not much to it.

she's got muscle cramps. she's very agitated. you see her twitching, a lotof restlessness, fine muscle tremors. and yup, you're seeingsome abnormal retraction of the eyelids, alittle bit of bulging of the eyeballs themselves. so thyroid storm. she's got way, way, way toomuch t3 and t4 in her body,

so thyroid gland is going crazy. so again, this can be extremeand very life threatening. so she is a medical emergency. she needs to go to the hospital. often precipitated by stress. she tells you she's taking herparamedic boards next week. nice. and it unfortunately doeshave a high mortality rate. i don't have a percent on that.

but it is high. so we're going to diagnose itthrough some very simple lab tests. we're going tomeasure tsh, t3, t4. what would i expect theresult of the tsh to be? tsh. it's going to be ok. yeah, it's going to benormal or low, probably low. because what doesshe have too much of?

t3, t4. so the actual thyroid hormone,t3, t4, is way out of control. so that feedbackmechanism, there's not going to beany tsh secreted. because the body wantsto shut down the thyroid. but it has no way of doing that. so here's her treatment. we're going to cool her down. because she's too hot.

she's 103.9. so we're going touse cool packs. this is something we cancertainly do in the field. pardon? is ok. because we're not worried aboutperipheral dilation and pooling blood. we want to bring her down. the challenge iswe have to achieve

a balance between coolingand preventing shivering. because what does shivering doto internal body temperature? raises it. so we might inducethe cold, that might, i mean, i've hadroom temperature iv fluids fordehydration personally and was shivering on those. so i would hate to know whata four-degree would feel like. so we're going toget fluids on board.

her glucose isgoing to be too low. t3, t4, the active formit has a lot of impact on many different body systems. so it impacts ourglucose levels. they're going to be low. electrolytes aregoing to be low. t3, t4 and is ahormone that does act on cardiovascular function. you can see howtachycardia she is.

so it's a stimulant. it's very much like epinephrine. so we may on board a betablocker to protect the heart and block that impact. she'll need glucocorticoids,because those are going to be too low. then the treatmentteam is going to have to decide which thyroidblocking medication they're going to use.

so ptu is an olderone, propylthiouracil, or methimazole. so those are the twochoices to kind of shut down the manufacturingprocess of that t3, t4. aspirin, very crucial notto give this lady aspirin. anybody know why? i always have to refresh myselfwith these little tidbits, too. the hormone, the thyroidhormone, the majority of it is protein bound in the system.

and then there's an enzyme thatcleaves it from the protein. and then that littlebit of free hormone is what's biologically active. aspirin cleaves that bond andreleases more bound thyroid to become free thyroidhormone that can now act. so we actually increase theamount of active thyroid hormone by givingthe patient aspirin, which is actually what wedon't want to do, right? we need to block it.

so this patientwould have aspirin as a contraindicationin all things. and that's the endof our eight cases.

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