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Session 4 - Live Rapid Review for BPS Exams

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This content is a comprehensive review of acute care and toxicology topics relevant to emergency medicine, presented by two healthcare professionals. It covers a wide range of conditions, from anaphylaxis and acute agitation to various toxicological exposures and their management.

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All right. Well, welcome everybody. It's

uh Dr. Busty and Dr. Cooko. We are super

pumped um about this session tonight

because it's uh all about adrenaline, baby.

baby.

I almost thought we would need some

intro music, you know, like some

something with some electric guitar or

something that was kind of up, you know,

really pumping you up,

>> but I was like, I don't want to make

anybody upset. So, but uh we're glad to

have you guys. Uh this session uh

tonight is going to be led by Dr. Koko

and I'm going to I'm going to sit back

and uh sip on my uh

my coffee and no just kidding. Uh we're

going to participate but Dr. Koko is

going to lead because the part of the

session is also toxicology for which Dr.

Co Dr. Cookio is the expert uh for sure.

Um, so we thought we'd give our, you

know, for those of you that are joining

us since this is acute, um, and critical

care, kind of emergency care, you know,

combination of those things. Um, you

know, our our backgrounds real quick.

So, you know, my training is u a little

bit different. I I trained as a a nurse

and a pharmacist and a physician, but in

nursing, my um interest uh was I first

got involved in uh surgical trauma ICU

care. uh and you had to do that uh spent

two years in surgical trauma ICU before

you could even go to the emergency

department. So uh that was back in those

old days. Um I then spent a year in

emergency department and fell in love

with it. Uh then went to pharmacy school

and did a lot of acute care and and u my

practice as well. But uh went back to

medical school and my my residency

training is in emergency medicine. I

still practice in emergency medicine. Um

and and I'm a critical care emergency

medicine kind of junkie I guess at

heart. Uh so that's my background. Dr.

Koko, go ahead and give us your

background and you know and and then you

can just go ahead and jump right in.

>> Sounds great. Yeah. So I'm a emergency

medicine clinical pharmacist. So yeah, I

mean I I had a I didn't have any similar

training in that respect. I definitely

wasn't a nurse and had that exposure

which it would be entirely forming and

interesting. But you know I went through

pharmacy school uh had rotations got me

exposed to the emergency department had

some other interests where you know I

was investigating that you know what I'd

like to do as a specialty during my

first year residency but really kind of

got tied and and fell in love with

emergency medicine uh in that respect uh

did my PGY2 and emergency medicine uh

later on getting different uh clinical

specialist roles in in uh my transition

from New York to Texas uh which has been

great. But along the way, one of the

things I always uh really enjoyed uh and

fell in love with was toxicology since

again training in New York, I got to

spend a lot of time at the New York City

Poison Center uh in their educational

seminars and just kind of getting to

know them. And if you know them uh in

any any capacity, Dr. Lewis Goldfrank is

the textbook and everybody who's an

author uh is actually a toxicologist and

an ER physician at NYU uh Belleview in

the New York City Poison Center. So I

got to work there, got to be a student

there. Um really got exposed and really

really fell in love with it. So uh

instead of doing a tox fellowship, I

actually decided to work as a ER

clinical pharmacist and kind of take my

own pathway studying for the the board

exam for toxicology. And then uh two

years ago uh I actually passed the uh

toxicology board exam, which is a kind

of different experience. Uh but it was

it was actually really great uh to kind

of get to that point in my career and be

able to uh check off that box just to

kind of make sure

>> the way I'm learning it is is definitely

the the right way and then be able to

obviously you apply that to patient care

scenarios. So, I mean, I still involve

the poison center every time we have a a

toxic patient uh that we're treating

just to get some collaborative decision-

making, but uh in the emergency

department is something uh I I do really

enjoy a lot. And the latest thing I've

been kind of branching into is

invenimations uh particularly with

copperhead snakes, which is what we see

a lot here in East Texas. So, that's uh

that's kind of what I've been doing. But

uh to start we're going to jump right

into uh you know emergency medicine here

in some different different uh care

capacities. So the the first thing we

are going to cover today and we're going

to cover quite a lot of acute care

topics is anaphilaxis. So we've talked

in the past about you know different

drug allergies but anaphilaxis is an

acute care emergency uh where patients

are essentially exposed to an allergen.

It could be, you know, any number of

different things, whether it's a

penicellin and a betalactim or a bee

invenimation or even a snake

invenimation or if we've just given them

an antidote. It could any number of

those things uh could you know induce an

mediated mass cell uh degranulation

that's causing all this different uh you

know immune response that isn't

necessarily necessary but it's an

excessive immune response leading to uh

swelling nerve stimulation excesses uh

numerous other capacities that are

essentially potentially

life-threatening. So uh what we

typically see in these patients as they

present to the emergency department um

they're complaining of puritis sometimes

some nausea rarely ever but mo a lot of

flushing if they have uricari it's very

indicative of what's going on there's a

numerous other symptoms that can present

as well if they're having chest pain

again if they have under underlying

cardiovascular issues that's going to

definitely incorporate that wheezing is

a big one that you'll see on physical

exam but one of the a few of the key

ones that we are concerned with that

were really screening for early on is

hypotension and if they have any

evidence of angria particularly in their

oral fairings or their airway uh which

is something very concerning for us that

we're going to have to intervene on

pretty quickly. So again what we find in

these patients again aside from this uh

you know hypotension and and angiodma

that's definitively forming is almost a

state of shock uh where they're having

yes these new you know novel cutaneous

symptoms but also having respiratory

difficulty hypotension uh and is just

unable to profuse critical organs. So

the key therapies that we have here are

I mean it's not what I would call rocket

science. Uh normally the way we approach

a lot of these issues in the emergency

department uh is it just a

straightforward ABCDE. So airway and

breathing assessing the airway the

patient able to talk or communicate uh

oxygenate their lungs oxygenate their

tissues. If they have circulation if

they have even a pulsate we can palpate

then we can measure blood pressure. Uh

the D is for disability. It's really a

GCS, but that's related to more trauma

patients explicitly, but we extrapolate

it in practical settings, just assessing

a mental status and expose the patient.

Again, we do that in trauma, but here in

in this scenario too, we do want to

expose the patient just to make sure

that we can identify any other potential

signs or sources of the aniflaxis that

we might need to intervene on. But aside

from that, uh early on these patients,

uh again, if we're assessing airway,

there's an issue, we're going to

intervene on the airway almost right

away. And at the same time, a lot of

these things are actually happening at

the same time. We're going to be

administering epinephrine as a key

therapy for this. So, one of the key

issues with epinephrine um that you I

mean, you do need to be aware of is the

dose in this scenario. So, it's not a

advanced cardiac life support dose where

we would give 1 milligram. This is a

lower dose of.3 to 0.5 milligrams uh for

adults. And we'd prefer to give this

intramuscularly since subcutaneous

administration although it's cited may

have some circulatory issues if the

patient's truly anaphylactic and you

know having a a persistent state of

shock. Again for pediatrics we do a 0.1

milligram per kilogram per dose which is

actually their uh ACL or PAL's dosing

which we'll actually talk about a little

bit later but really we do have some

ancillary therapies but airway and

epinephrine are kind of the definitive

care that we can give for these patients

that's going to intervene right away.

The other therapies like dyenhydramine, corticosteroids

corticosteroids

um are really used but we use them in

the sense that they are going to uh have

a onset of action in about six hours. So

we can stabilize the patient but if we

can't take care of the thing that's

causing the aniflaxis is going to recur

but those steroids and uh antihistamines

can actually hypothetically prevent a

recurrence from occurring. So that's why

we try to give them quite early on.

There's some other therapies that we

could hypothetically give uh if we don't

have introvenous access like albuterol

uh early on and that's really just going

to allow us to uh uh you know give some

uh catakolamine response to the patient

not necessarily bronco dilate uh but it

is a key thing that we are going to make

sure we're doing.

>> The thing for you guys also need to

remember is disposition. So if they come

into the emergency department and you

just give them one round of epinephrine,

steroids, you know, H27 antagonist,

whatever those other things that are

really for trying to prevent the

secondary flare, uh they have to stay

for at least six, maybe even up to eight

hours, but a minimum of six hours. And

if you because that's when the drugs are

going to wear off and if they wear off

and they you send them home and then

they go in aniflaxis again, then they're

you know, you're in trouble. So that's

what you're trying to discern. if they

get a second um dose generally at that

point you have to very give strong

consideration to admission u because

obviously the allergen is sticking

around and they're having rebound um so

disposition is important and then when

you also discharge them they need to go

home with prescriptions that have you

know two pens of epinephrine steroids I

mean the treatment doesn't end

>> right when you discharge them it

continues on because again that allergen

is probably going to be present all

right let's move on

>> absolutely absolutely Absolutely. So, uh

let's see if I can go forward here.

There we go. So, uh acute agitation is

another common thing we actually see in

the emergency department. We do see it

in numerous other capacities, but this

is really, you know, pertaining to

patients that are uh having some

underlying psychiatric uh you know,

issue going on that there's an acute

exacerbation uh in their emotional state

that's re you know, emerging as

agitation. but also it can be really

related to an excessive sympathetic

activation um even through pain

activation or pain perception. So what

we're seeing in these patients is a

pretty complex central uh nervous system

pathway that we do have to try to

intervene on pretty quickly. There's a

number of different pathways that have

been suggested uh that we manage these

and they have evolved over time where

we're not necessarily just trying to uh

calm down the patient even though that's

what we're trying to do early on. try to

have some verbal communication. Um,

intervene as much as possible. If there

has been an escalation in anger or

aggression, if they're hostile, uh, you

know, those things are somewhat

intervenable through psychiatric care.

Uh, but in acute care settings, we don't

really have access to psychiatry. We're,

you know, the intermittent providers

trying to intervene on these patients.

So, we're going to do what we can. Uh

but if there's a state of violence or

they're aggressively resistant, we do

hypothetically have to escalate the care

that we're giving to try to consider

some drug therapy um to intervene on

these patients. The the kind of balance

we're facing in this scenario is to

determining whether the patient uh can

swallow. If they can swallow and they're

willing to take medication at that time,

that's excellent. Uh we can try to give

some benzoizipines usually first line.

If not, there's some antisycchotics that

we could administer. uh orally in these

scenarios. A lot of times we still use

the uh first generation or older agents

like haliperidol uh as an oral agent. Uh

but we have evolved to some of the other

uh newer agents which have some ODT

formulations like olanzipene which we we

can give actually pretty effectively

orally. But if a patient isn't you know

compatible or isn't compliant with an

oral administration of an agent at that

point that's when we're looking at

parental. So again if they have IV

access great but most of the time in

these scenarios we don't have IV access.

So we're going to be administering these

drugs intramuscularly.

So uh again troperol or haloparidol are

considerations in this scenario.

However, again some of the uh modern

shift even though those are totally

effective uh we can use some of the

newer atypical agents like olanzipene uh

aeroprizole or ziprazadone all come in

parental formulations but I mean those

are definitive uh agents we can use but

almost first line all the time we were

giving benzoazipines to try to have this

patient's acute agitation taken care of

um you might have heard or seen in

practice uh there's a I don't want to

call an algorithm but it's a it's is an

analogy of a B-52 which is a combination

of benadryil or dyenhydramine uh 5

milligrams of heliparadol and 2

milligrams of larzopan and that

combination had often been kind of

disregarded downregulated um kind of

looked upon critically in numerous

circles because we you know thought it

wasn't necessarily the right thing to do

or superbly effective over other

interventions but some studies have

actually come out in the emergency

department setting actually

demonstrating this is actually a fairly

effective uh and safe combination to be

using these patients and since we can

kind of take advantage of a few of the

other um uh uh I guess

complex drug interactions that are going

on that are somewhat beneficial for

these patients. But again, oftentimes a

lot of these things are considering uh

the patient in in this acute environment

and it can get pretty um go pretty

quickly uh pretty pretty fast in in

numerous scenarios and we can get the

patient under control. if there was any

reversible issues we could identify

that's usually happening after we've

gotten the patient stabilized. Okay, so

moving on to anti-coagulation reversal.

Um this is something we do see in acute

care settings usually related to an

acute hemorrhage that's going on with

the patient. Uh there are ex you know

other circumstances if a patient needs

acute care surgery for some other reason

other than hemorrhage but they're on an

oral anti-coagulant outpatient that

they're coming into the hospital for. We

are going to have to intervene in that

respect also. But the the antiquated way

we used to deal with this is when we

really only had one oral anti-quagulant

outpatient which was warren. Uh and in

that scenario we would give uh vitamin K

with either uh fresh frozen plasma or

FFP uh or a what we've evolved to even

in that sense a uh PCC which is a

prothrombin complex concentrate. um and

even in we've had some other scenarios

where we've given other uh coagulation

factors but those have been proven

harmful but nowadays since we have the

doax available so we have a combination

of the direct 10A inhibitors and we also

have direct thrombin inhibitors there's

been market uh uh penetration of

specific agents to treat that. So again,

a lot of this has to do in determining

what to do is getting a good patient

history. Uh if we can identify what

they're on as an outpatient to intervene

upon and then identify again if there's

the indication. So whether it's an acute

hemorrhage or if it's merely a reversal

of the agent to per you know allow a

certain procedure to go forth. So once

we've identified those factors again

identifying what agent the patient is

taking then we can really further

identify exactly what the reversal agent

is. So I already kind of described with

Warframe what we're going to do. It's

largely vitamin K and a PCC and in

determining the route of the vitamin K

it has to do with essentially your time

and desired onset of reversal. So if

they have a life-threatening acute

hemorrhage, uh we are going to likely

use a parental form of uh phytonion or

vitamin K. And in that scenario, we're

again dependent on the INR in many

scenarios, you're going to have

different dosing. But if it's a

life-threatening hemorrhage, you're

usually almost always giving 10

milligrams parentally, usually through

an IV infusion. And uh if the patient

isn't necessarily acutely hemorrhaging

and we can identify which INR the dose

of the uh fitonadino might differ again

depending on that INR anywhere from

about 2 milligrams again up to 10

milligrams. Now we we give the the

vitamin K and again kind of reflecting

back to some of the other things we were

just talking about where its time of

onset like a cortosteroid and aniflaxis

is actually not immediate. it's going to

take at least you know two to four

sometimes six hours for an oral agent

oral administration of vitamin K to have

an onset. So if you have an acute

hemorrhage you need to give something

that's going to work immediately. So

that thing is usually PCC or prothroin

complex concentrate because it has four

of the main clotting factors 279 and 10.

And again this scenario we do uh deeply

consider factor seven since that's a

major issue uh specifically in a lab

sense with warfin. So we're going to be

reversing that by replacing those

factors and then we're going to have an

immediate reversal of the INR and again

hopefully that's going to clinically

relate to acute uh control of the the

bleeding going on. Now if they're on a

DOAC something like a direct throman

inhibitor there uh you can use uh again

FFP you can use PCC's like Kentra uh but

there are other novel agents coming out

like indexinate alpha which have been

directly developed for this specific

agent and the way you think about those

agents again they're essentially uh

inactive factor 10 molecules that the

these drugs can bind to and essentially

become inactivated so they're not having

their systemic anti-ta

effect anymore. So we can give that

agent in that scenario to try to

specifically reverse those agents. And

then with debigatran there's a specific

reversal agent for uh that medication

called praxvine by the brand name or I

dare useab uh which again is kind of uh

you can think of it again as a monoconal

antibbody. So it's kind of going into

binding up the available debigotran

preventing its action to go forward. So

depending on the patient depending on

the scenario that's when you're going to

be able to determine exactly which agent

of these are going to give. Now dosing

is quite complex. I wouldn't expect

you'd actually see that on the BCPS exam

since again although there's package uh

labeling dosing the clinical dosing

we're giving in these scenarios is is

actually quite different. Um so having

that in an explicit exam question

actually I don't think they would be

able to do successfully to make sure

it's a legitimate uh board review exam

question. So uh moving on to carbon

monoxide exposure. So carbon monoxide is

a product of essentially combustion. So

if uh you are in uh and also carbon

dioxide is as well, but if a patient has

been exposed to a fire uh or a house

fire, something combusting or otherwise

in a chemical facility that has a

byproduct of carbon monoxide, they could

be exposed to this and it actually has

quite um delirious and definitive

effects where it it decreases the

ability of oxygen delivery to tissues by

essentially binding to hemoglobin and

resulting in the inability of that

hemoglobin uh to dissociate its oxygen

to those cells. So, one of the key

things we can identify in acute care

settings is uh if you can get an AVG and

a VBG and if the PAO2s and oxygen

concentrations are actually the same in

the ABG and the BBG, you can actually

tie this to a carbon monoxide exposure.

Again, if they come from a scene where

there could have been a carbon monoxide

exposure. Uh on most modern blood gases,

you actually do get a caroxyhemoglobin

level. um which uh you can see here

there's normal therapeutic levels that

you might see especially in someone that

is chronically smoking outpatient.

They're going to have a normally higher

level than someone like again I don't

smoke so I would have a normally lower

uh closer to the normal range but a

smoker could have anywhere from a 9 to

10 sometimes 15% caroxymoglobin level

but we do start to see uh some CNS

changes in some of these carbon monoxide

clinical effects in patients that have

been exposed and have these high

caroxyhemoglobin levels. So to intervene

on these patients drug therapy wise it's

pretty limited. There's really no

definitive drug therapy. We're just

going to administer oxygen to these

patients as much as possible. Now in so

modern and this is actually quite

debated. I don't know if Dr. Buskai

wants to chime in. It's not drugrelated

but hyperbaric oxygen has been brought

up as a therapy that we deliver for

these patients since it can improve

oxygenation and help remove the carbon monoxide.

monoxide.

Not every hospital has it and some

clinical evidence with it is

>> hard to I guess

>> not to find but yeah

>> you're in a tough bind when you when you

find somebody in this situation because

you don't have many options and so if

someone's having chest pain especially

if they're underlying cardiovascular

disease and they're having an MI as a

result of the eskeemia then you need to

you know do whatever you can and you may

have to transfer them to a center that

has this capability so that influences

your disposition. The second patient

population that you have to keep in mind

with this uh is pregnant patient because

it's not just the the patient but it's

also the the baby the other patient. Um

and so any degree of lack of oxygenation

is important. So hyperbaric oxygen

therapy theoretically increases the

elimination by changing the you know

halflife a little bit of it. But you

know it's better than doing nothing. So

if you have access to it you you know

you should do it. All right.

>> Absolutely. So uh speaking of babies uh

and pregnant mothers uh again this is

something we do see in the emergency

department actually fairly frequent I

don't want to say frequently but we do

see it and it's something that we all uh

kind of intervene on but uh with a

pregnant patient >> sweat

>> sweat

>> they don't like seeing pregnant patient

the emergency department like no no no

go to ob

team down to the ER and then we're all

in the same boat anyway it's usually

pretty collaborative to work with them

at the same time. But uh we do see some

of these emergencies with our pregnant

patients. Again, we kind of loop them

together whereas with eclampsia and

preeacclampsia, but there is some uh

definitive uh differences between the

two, but largely we can group them

together in this context. But

essentially the whole concern is that we

have a reduced blood blood supply to the

placenta causing some uh increase in

arterial resistance and vasoc

constriction uh where the the fetus is

uh you know the the fetus is still

inside is having some oxidative stress

and potentially some eskeeia. Now that

effect is certainly dangerous to the

fetus inside but also hazardous to the

mother uh which all these systemic

effects are you know propagating and

presenting in in in very discreet

fashions in very you know emergent

fashions. So what we see in these

patients is they often present usually

just not feeling well or having some

belly pain, chest pain, even some uh you

know uh symptoms that might suggest uh

early uh labor, but in reality we can

identify these patients pretty quickly

or not necessarily pretty quickly uh but

we can identify these patients. Um again

they're going to have acute hypertension

which is a key thing that we're going to

identify here. You might recall just

from hypertension guidelines or or

hypertension uh therapeutic

decision-making there are certain uh

levels and parameters we look at

specifically for pregnant patients. But

again having any underlying ultrammental

status uh if they headaches seizures uh

seizures are definitely something we're

concerned about in these uh patients.

We're going to want to intervene pretty

quickly uh on these uh uh uh patients.

And one of the again key interventions

is again not drugreated but it's uh

whether or not the patient can have an

early uh uh essentially uh delivery of

the fetus and we're going to get OB team

that's why they're kind of coming down

to help manage those patients but

otherwise some of the early acute care

measures we can do to try to account for

largely the hypertension is not

necessarily jump straight to you know

vasodal dilators like we would in acute

stroke patients but we're going to

actually treat with magnesium uh almost

straight way and the magnesium dosing is

quite high. Uh, and it's a good kind of

analogy to acute asthma exacerbation

patients where oftent times our our care

systems often limit how much magnesium

those patients can get like one to two

grams and then we have to kind of

downplay their therapy in a in a context

but we try to you know in my practice I

try to relate those patients to you know

preeacclampsia clampsia patients where

we're giving 5 to 10 grams of magnesium

sulfate uh to a patient almost right

away usually within we try to at least

delay the infusion about 10 to 15

minutes because it does cause some

vasoddilation, but we're getting this

magnesium on board very very quickly to

try to uh vasoddilate the patient and

provide some relief in and you know

profusion to the placenta into the uh

indwelling fetus in that in that

respect. So if we don't have IV access

at the time, we actually give this

intramuscularly and the the site of the

intramuscular injection is actually the

glutial tissue. Uh it's it's it's too

large of a volume to really go in the

deltoid or even in the thigh. So we do

it in the glutial tissue and you do five

grams in each glutial

I guess cheek I guess if you want to

think about it in that respect but if

you do have IV access we are giving it

pretty quickly and then it continues as

an infusion at about 1 to five grams per

hour and you just try to titrate that uh

usually alongside of the uh the OB team

at hand but again if we can't get that

blood pressure under control with the

magnesium we do jump to our vasodil

vasoddilator therapy which is largely

related to ledol nicartene uh in this

diff in this specific clinical scenario.

So uh there are some second line agents

you might have seen in uh older

literature or older textbooks they use

uh uh methyl uh uh I want to say like

hydraazine yeah and methylopa in this

scenario but it methodopa we really I

haven't used it in maybe five maybe 10

years uh clinically and I haven't seen

it stocked in the pharmacy department.

I'm sure there's some odd o use of it

that we retain it but it's really not

used clinically anymore. uh secondarily

hydraazine is also secondarily

referenced in some of the old uh

textbooks and literature but although it

can be used acutely we actually don't

prefer it because it has this odd uh uh

dynamic onset of action and duration of

action for a patient and what I've seen

clinically is that some patients and is

very difficult to present and predict

who this is we can give a bolus dose of

hydraazine about 20 mill or 5 to 10

milligrams we wait 20 minutes to recheck

their blood pressure nothing's happens.

So we give another five, nothing happens

and then at an hour all 10 milligrams

hits them uh and they're they get very

vasoddilated very acutely and they get

hypotensive and in almost a shock state.

So it has this very odd unpredictable

onset of action that we really don't

prefer it unless we're in a specific

scenario where a patient otherwise can't

tolerate it or can't take it for some

reason. Um but uh we'd reserve it for

that. And again on the inpatient side to

kind of continue this management uh if

they're on the OB floor they're probably

going to get continued on an oral uh

nephetipene regimen to make sure that we

can control the blood pressure at that

time. But again magnesium and then as a

basil dilator is a key therapy here. And

again we're going to be giving it

rapidly uh which is something a little

bit um somewhat unnerving at the at the

start for most pharmacists but you can

actually get pretty used to it if you've

seen it in in numerous different

capacities. Now related to these OB

patients, there is a a secondary uh uh

you know risk after delivery which is

something called postpartum hemorrhage.

So again the the the name of it is

somewhat obvious related to what's going

on is that they have an extra you know

an inability or inadequate concentration

or contraction of the uterus that's uh

not allowing either the uh hemostasis to

occur after delivery uh or some other

factor related to underlying uh

hematologgic disorder that the patient's

got underlying uh that otherwise hadn't

been identified or hadn't been poorly

managed or otherwise we can't manage

until delivery in these scenarios. So,

uh, they're going to have, you know,

extensive hemorrhage after delivery of

the of the the the new baby. So, in this

scenario, oftentimes it what we see in

these patients is pretty obvious. We're

seeing a lot of hemorrhage, but also uh

shock related symptoms that are going on

with the patient in in the acute

setting. So, they're going to be uh

veagal, they're going to have

altermental status, maybe other

neurologic deficits related to lack of

profusion like blurred vision, uh creamy

skin, if they're going to be tachocartic

or typnic, trying to oxygenate those

tissues. That's something we're

definitely going to see. Um, and again,

the treatment in this scenario is not,

you know, overly shocking in the sense

that we do need to replace their blood

uh in this scenario. So, tight cross

matching and and and identification

which blood product is more appropriate

for them. But in general, OOS or O

negative would be ideal to at least

empirically use. uh but uh we do want to

extend our therapy to other agents

including uh trans tr transexemic acid

uh and some other OB agents that you

might see in acute care settings like

oxytocin moprotool and ether uh or

gonavine. So those are a kind of a

cocktail that you might see in uh acute

care settings in the hospital setting

after a delivery to control the uh

postpartum hemorrhage. But uh one of the

agents uh we can actually uh kind of

take a caveat on I just want to uh we

we've talked about transmic acid. We're

actually going to talk about it later

related to trauma. Um actually maybe

we'll relate after we talk about with

trauma also to kind of answer a question

that was posed to us uh earlier on uh

before we got to this session. So again

with this with this sorry go ahead Dr.

>> No. Yeah. So the thing that's, you know,

about postpartum hemorrhage, I mean,

it's non-farmacologic as quickly as

possible. I mean, basically,

>> I hate to say it, but you just stick

your hand up in the uterus and you

massage it. So that's what that by the

manual uterine massage. You get that

thing to to spasm essentially as quickly

as possible. And so you're rubbing on

the super pubic area, the uterine wall

on the outside, and you're just getting

it to contract. The next thing that you

can do is just shove some isoprosttol uh

into the vagina itself. and those

prostaglandon analoges will start to

cause um contraction. If you have

oxytocin hanging, that's clearly the

thing, you know, uh hit it. So, as

quickly as you go through those things,

that's what you're going to try to do.

In most cases, it can work. If you have

to, you can always stuff um gauze or

other things in there. So, anyway, all

right, let's move on.

So uh just jumping on to so

hyperothermia and oftentimes we've seen

again in numerous different disease

states largely infectious disease as an

one of the initial presentations that

could patient could be hypothermic but

considering it in a different context

almost as an exposure to heat itself. So

patients again we we do see this here in

Texas but you might see it elsewhere in

the country depending on you know at any

point they could be from their job site

where they get exposed to quite a lot of

heat uh either from a furnace or some

other device like if it's a a smelting

plant something like that they could be

exposed and there's a range of different

syndromes that they can present to the

emergency department with uh that will

you know are are somewhat interesting in

kind of a a spectrum of of an acute care

setting. So these patients can uh you

know have anything from heat cramps,

heat exhaustion uh to what's called a

heat stroke, which is somewhat of the

most severe scenario uh in this setting.

So in these patients with heat cramps,

again, it's kind of indicative to the

the name of what's going on is that

they're just going to have these uh

muscle cramps in their thighs and and

present with a high baseline

temperature. And oftentimes we can see

this from you know people exercising

outdoors or being in a different

capacity even after a road race

something like a marathon uh where

someone may maybe not necessarily

trained as best as they could and have

done it in somewhere like a hot

environment or in the summer and now are

presenting after the race because

they're having excessive heat or

excessive cramping in those tissues. uh

and we can relate this to something like

rabbomiolyis which is going on. But in

this scenario these patients are

otherwise underlying pretty healthy and

can manage this but uh they it can

escalate even further to that uh to

something called heat exhaustion where

again we've kind of taken it from the

heat cramps to now they're actually not

just feeling fatigue from a the work

they're doing or the race they've been

in but actually fundamentally uh you

know lacking energy entirely. So they

could be ataxic, they could be dizzy,

they could have impaired cognition, um

headache, malaise, other numerous other

symptoms that are actually quite

concerning that they're not just tired.

There's actually something legitimately

wrong going on with this patient all the

way to heat stroke which can present

almost exactly like an acute stroke uh

which could be thrombomolic or

hemorrhagic presentation where a patient

has definitive alternal status. They

could be hypotensive uh hypotensive

tacocartic uh with uh some rapid

breathing as well to try to you know

oxygenate and eliminate some carbon

dioxide but they can also have a pretty

wide pulse pressure in these scenarios

too. So in order to manage these

patients obviously we try to have to

identify and rule out other causes of

their uh hyperothermia. But again if

based on their history we can identify

they were definitively exposed to heat.

Uh the easiest thing to do is actually

cool the patient down. And uh again in

my in my various practice settings I

again even though I was in New York

which is not as hot as uh in Texas but

there was a lot of drug use that related

to you know poor heat management these

patients we would actually have an ice

bath in the emergency department where

the patients would literally get uh

dunked into the ice bath if they had

intact airway uh to try to cool them

rapidly. But if that you don't have the

ice bath in your emergency department or

qare setting, you can actually do a

topical cooling therapy with ice packs

or cooling blankets which are available

in many emergency departments now or in

a qare setting. So try to utilize that

and also we stock uh normal saline uh in

the refrigerator to usually a

temperature of about four degrees

Celsius uh to make sure we can actually

infuse that introvenously for the

patient as well to try to cool them down

as rapidly as possible. and anything

else we can do supportively. So again,

they're having seizures. If we can work

them up for an acute stroke, we can get

them stabilized and have a CT scan after

that to, you know, kind of confirm that

there isn't anything else going on

internally. Uh then we'll kind of pro

proceed with that. Um but again not a

heavy drug therapy thing. But one key

thing here is that you might identify is

actually storing the uh saline or

lactated ringers in the refrigerator uh

in almost close to the freezer but in a

very cold section of the refrigerator to

make sure we can actually administer

this uh introvenously to these patients.

So it is something to actually uh kind

of think about uh either practically and

also in during the exam. Now the flip

side of that is hypothermia. So this is

again something if again I'm actually

originally from Canada uh even not that

far north of Canada but something you

know you might have been exposed to or

heard about in the news or the

literature even where patients exposed

to very cold temperatures uh can present

to uh you know you know in in a in a

shock setting in by lowering their core

body temperature uh fairly low that can

actually prevent uh circulation in in

numerous different organ functions that

also lead into shock. Now these patients

are actually quite different in terms of

how we manage them. So although they

present to the emergency department with

this uh alternal status uh potentially

arhythmias and uh decreases in cardiac

output uh what we're doing for them is

warming them but trying to warm them you

know fairly quickly but not over

aggressively and uh we try to target a

normal not necessarily a normal

temperature but getting towards a normal

temperature fairly quickly in these

scenarios. Now, one caveat to this is

that if you have a patient presenting to

the emergency department or an acute

care setting that is in cardiac arrest

and they are hypothermic, so they are

found in the water or found under ice or

found outside during the winter, we

actually have to continue the

resuscitation of this patient until we

actually have achieved uh somewhere

close to a normal body temperature where

we have to essentially resuscitate them

and uh until we've resolved this

hypothermia to make sure that we can

actually assess them appropriately in

that scenario. So the rewarming method

is that we administer again this is kind

of the opposite. So instead of a cooling

blanket we put a warming blanket on

them. We put as many uh warm uh devices

that we can that are accessible in the

emergency department. Usually those uh

warming blankets. Other blankets you

just might have lying around getting

them in a warm room. Usually the

resuscitation base if it's a trauma bay

is kept at a fairly warm temperature uh

anyway. So it's a good place to have

that patient definitively. And then on

the flip side from cooled saline, we

actually have warm saline that we can

give to these patients as well. Uh that

can be infused fairly rapidly to try to

get a systemic response for these

patients. So it's kind of uh again it's

obvious that's a flip from a

hypotherapy, but the clinical management

in in the perception is actually uh

somewhat different. I don't did you have

something to comment on, Dr. Busai? No,

I mean I mean most of the time we will

use bear huggers and stuff like that to

raise it in warmed uh saline. The other

thing to keep in mind is on a

differential diagnosis is you can also

see this in patients with significant hypoglycemia.

hypoglycemia.

Um so it's not just a thermal issue. uh

hypoglycemic patients can present

hypothermically as well and it creates a

you know a confusion a little bit in in

patients and they're hard to get u up

until you also facilitate their blood

sugar correction. So

>> right yeah so also again reiterating to

resuscitation if you recall our your hes

and t's this is something that uh can uh

you know incorporate into your kind of

assessment during that those acute care settings.

settings.

Definitely. So, uh, one of the other

issues again if if say you resuscitate a

patient like that, uh, and they are, you

know, destined to be in the in the

emergency department and likely in the

intensive care unit, one of the key

parameters we actually use to help

support these patients is something

called managing their pain, agitation,

and delirium. Now, the SECM, which is a

society for critical care medicine, uh,

puts out these guidelines, the PAD

guidelines. They used to be called

something else but we've kind of evolved

our nomenclature and a reference to it

to kind of reiterate that we are trying

to take care of three main issues that

are going on with these uh critical care

patients. Now uh pain and agitation are

a little bit uh a little bit predictable

because again a pain a patient that is

intubated has numerous IV sites for

lines if there's a a clinical syndrome

going on that's related to you know

discomfort and pain we're gonna have to

manage that uh definitively. But also

agitation is something that can occur

just because the patients are in a

hemodynamic complicated state that's

producing a lot of emotional stress and

emotional distress that can result in in

some agitation. But delirium is

something you might see in a prolonged

uh ICU stay where it's kind of a

emergence of an altermental status from

poorer management of you know pain and

agitation. So in order to try to manage

this again we what we try to do is you

know identify you know the pathways in

the the individual patients that we can

intervene upon with the pain. So if

there are different regimens we can

utilize whether it's a nonopioid based

therapy so utilizing acetaminophen uh

for these patients optimizing that if

they need local anesthesia uh for

different procedures that are going on

or escalating it to opioid based therapy

uh we can definitively try to make sure

that they're getting a definitive care

for these patients with agitation. Also,

again, it can relate to not just drug

therapy, but also making sure that the

patient is on a hypothetically a a sleep

or awake cycle that's appropriate,

trying to support them emotionally

through other different care measures.

But again, if they are becoming

agitated, somewhat related to the acute

agitation that we've seen previously is

that there are antiscychotics that could

be administered. Otherwise, we're trying

to identify how to optimize their drug

therapy in other capacities uh to try to

prevent the progression to agitation

itself. Now delirium is kind of an

exacerbation of of the previous two

where the patient is having definitive

altered mental status related to uh the

agitation and pain that are they're you

know experiencing in the in the either

the emergency department or the

intensive care unit. And a lot of this

is somewhat of complicated therapy. Now

back in the day when I was training a

lot of this was related to what we used

to manage this was hyaloparidol at

escalating doses. And what we found with

that of course if you can remember with

haliperidololis it's QT prolongation and

and definitive risk with that as you

escalate the dose. So a lot of

interventions have been tried to be

evolved that are going to optimize that

with different antiscychotic or

different optimization of other drug

pathways but it is still actually

somewhat reserved in different

capacities to try to address their

agitated state and prevent any

progression of delirium. Now again the

guidelines kind of go into depth about

uh the the causes and issues related to

this but all of it really ties back to

and what to do pharmacologically to

basic drug therapy. So again as you can

see here treating pain if we can use

fentanyl uh that's likely what or uh

hydromorphone or hydrocodone those are

somewhat of the uh more ideal opioids in

this setting just because specifically

with fentanyl again in an acute care

setting it's not going to cause any

histamine release uh and it's going to

have very limited uh vasoddilation. So

if a patient's hypotensive or has a

shock state it's going to limit that

from progressing. But there are other

issues that can cause respiratory

complications. So it can cause some uh

ridging or uh contraction of the

ventilatory muscles that is somewhat

concerning. Uh but for agitation we just

want to make sure that patients on

appropriate sedation uh and sedation

holidays if we can in certain capacities

that are appropriately managed. So with

these guidelines, they do recommend

propal or dexitodine as first line just

because benzoizipines aren't necessarily

bad sedative agents but just like with

alcohol you can actually have withdrawal

from these agents if it's not

appropriately managed but can uh

manifest as delirium. So you just really

have to optimize the drug therapy as

best as possible in these scenarios

which can be uh uh complicated. And it's

not definitively easy in the ICU setting

to and identify the best sedation uh

process for every patient but it's

something we do try to um identify for

most patients. Now uh rapid sequence

intubation actually is the process in

the in the whole procedure that we

utilize to secure a patient's airway. So

if you recall uh back when the the first

discussion I was having with aniflaxis

we talked about ABCDE

uh and airway is really the first step

in managing a lot of these patients. So

with securing the airway, if the patient

can't talk, they can't ventilate, they

can't oxygenate, uh they have an altered

mental status, we're almost always going

to be intubating the patient acutely.

And this differs from controlled

intubation, which you do see in the O

setting uh quite often, but in where you

have a very controlled environment, it

can go very slowly. You have a

identification of everything going on

with the patient including baseline

labs. Rapid sequence intubation occurs

in again this acute care environment

where we might have not have anything

related to the patient and we may not

know their name uh but we have some

basic history of what's going on

hypothetically and we can do a very

rapid uh primary survey of this patient

and if we you know deem that the patient

needs airway support we're going to go

down this RSI sequence and it's really

been divided into seven uh ps of RSI so

we prepare uh the situation as much as

possible getting and identifying which

drugs are going to be used uh for the

intubation, which devices, which people

are needed, and where it's going to

occur. Again, hopefully in the emergency

department or another acute care

environment, but it can even happen

prehosp. We're going to try and

preoxygenate the patient. Again, likely

uh we're going to preoxygenate them as

much as possible, but there's some uh

competing literature as to whether or

not this is definitively safe because

sometimes we see high levels of

preoxygenation um just you know giving

them excessive oxygen, but we know that

can be harmful in certain cardiac

situations. Uh so it is something we do

consider in in many patients, but it's

really up to a team decision. We try to

pre-treat them and that was one thing we

we used to use a lot of uh and there was

an acronym uh called lean uh which was

uh or or load in some capacities also uh

where we would premedicate the patient

but that's kind of fallen out of favor

in numerous capacities. But then that's

it. The next P is kind of where we get

into the main treatment therapy for

these situations which is paralysis with

induction. And although we call it

paralysis with induction because this is

7P pneummonic uh we should actually be

making sure to sedate the patient before

uh we paralyze them. So the induction of

sedation is utilized with very potent

very rapid acting sedative agents. The

ideal agent here is acidate in many

capacities. second line agents include

ketamine, propylall and even

benzoizipines in some scenarios uh that

we're going to administer to these

patients where they have a 30-cond maybe

45 second onset of action. Uh and then

we're going to paralyze the patient

either with a depolarizing neuromuscular

blocker like suininal or a

non-deolarizing neuromuscular blocker uh

like rockuron rockuronium or beeronium

in these scenarios. Uh so after the

patient's been sedated adequately and

paralyzed uh the uh ED physician or even

an anesthesiologist that might be uh

coming down to help with the airway is

going to help position the patient to

you know visualize the airway uh place

the tube through the larynx and and also

definitively identify if it goes through

the right channel to make sure we can uh

see oxygenation going on in a carbon

dioxide exchange. uh and then post

intubation management that's where the

pain agitation delirium kind of steps in

where we try to sedate the patient and

provide some analesia

going forward with them. So uh before

jumping into trauma I know that was a

lot of topics in acute care setting but

uh Dr. Busty was there anything you

wanted to jump in on before we head into

trauma? Yeah, for RSI, I think that, you

know, where they might um want you to

recognize neuromuscular blockers is, you

know, if you have a a airway that you're

not sure that you're going to be able to

secure or because not all airways are

the same. So, if you got a big neck or

short neck and uh some airways are

difficult, then you need to have backup

measures and you can use LMAs and other

things like that. But a nice thing about

suininal is it will wear off and you can

at least then try to regain some of

their you know your ability to ventilate

and oxygenate the patient if you have to

end up doing it manually or you need the

drug to wear off. Rocky roniums can

obviously stick around a little bit

longer. Theoretically and historically

people used to teach that you can't use

sueninal in you know traumatic head

injury or patients with hypercalemia or

significant third degree burns or CKD

where hypercalemia could be present and

that's all stuff that is somewhat true

and relevant because when you have

contraction of the muscle you're going

to elevate the potassium for a very

short period very subtly but most of the

time that that's not based off of really

strong literature um and it doesn't mean

that you can't but from a board exam

perspective that you probably they're

probably trying to get you to use

something else um at some level because

you don't know it's because you're not

going to have immediate labs available

to you right away.

>> Um so just kind of keep those little

nuances that we teach versus what really

happens in the in the clinical world.

The other drug that can be used as

sedative especially if somebody is

having respiratory distress from an

asthma you know asthma or bronospastic

problem is ketamine. So ketamine can

offer a little bit of a broncoilatory

effect and still achieve neutral

hemodynamic influence um and uh the

sedation that you need. So I think we

got about 10 more minutes and then we'll

take a break.

>> Yeah, that'll give us a good opportunity

to go through some uh trauma topics. And

again, trauma is is, you know, an acute

surgical emergency and there's not a a

tremendous amount of drug therapy, but

the drug therapy involved here is

actually quite substantial, even though

it's not overly complex. So, we're going

to go over some of the key parameters

here and key topics that you should be

aware of that could come up in in

different capacities. So, one of the

things we do have to consider in in a

tra traumatic injury that is an exposing

injury of other tissue or organs. So if

it's a uh you know grade two or three

open fracture which is a fairly large

fracture where you're seeing the bone

come through the tissue or have a large

laceration that's exposing uh you know

gut tissue or other you know various

other intra intraabdominal or

intrathoracic or any uh you know secured

physiology that's going on. we are gonna

hypo and definitively want to give the

patient antibiotic prophylaxis before

they go to the O for definitive uh wound

uh cleaning and closure. And you could

kind of relate this to how you might see

patients being managed uh prior to a

planned surgery where we're getting

antibiotic prophylaxis before the

incision is made. Now in trauma, the

incision has been made uh in in an

outpatient setting and now we're just

trying to intervene on them. So the drug

therapy isn't overly robust in terms of

complexity where we often use uh

betalactams like syphaselin as a

firstline agent or a firstline uh drug

therapy consideration for these patients

and dosing is somewhat of a emerging

knowledge base where we're trying to

evolve it. So most of the time we would

often default default to one gram of

sephaselin for many patients but anybody

over uh 60 to 70 kilos usually 70 kilos

we're giving at least two grams. If

they're over 100 kilos we might give up

to three grams of sephaselin in acute

care settings to make sure that we can

get them appropriately managed. uh now

if in certain scenarios if they have an

open fracture which I will touch on

later they get an extended uh drug

therapy uh regimen which we'll kind of

go on in a little bit later but one of

the key things here is that if you

identify a patient with a betalactim

allergy uh some of the key drug

therapies again if we can't definitively

rule out what the actual allergy is we

kind of have to default to a

hypothetical risk where we don't want to

hypo you know cause further vasod

vasoddilation with this patient uh We

don't want to cause further hemodynamic

compromise. So we're going to defer to a

second line agent combination which is

uh clintomy with or without metronidazol

but often we use it as a combination and

once we can get these drugs administered

to the patient um we can hopefully get

them to the O and get definitive wound

closure and clean cleaning uh before

anything kind of extrapolates from that.

So again, it's not uh you know terribly

complex drug therapy, but getting a good

patient history with allergies is

actually somewhat prevalent. Also making

sure we're getting the appropriate dose.

Now also in this these traumatic

patients, they might get uh a large

volume of blood uh profused to them

because they're hemorrhaging quite

extensively. So uh we call this massive

transfusion usually when the patient's

getting uh four or more units of path

red cells within 24 hours. And in some

settings you might think that's uh a lot

but in acute hemorrhage that's actually

not a lot at all. Uh we get into massive

tri transfusion quite readily in in in

acute care settings. And just kind of

caveat with that in detailed thinking

one unit of packed red cells is about

250 cc's. And if you can think of the

average American adult we have a

intravascular volume of about five lers.

So if we give four uh 250 cc packed red

cells that's giving one liter. So that's

about 20% of your intravascular volume.

So if you've lost 20% of your

intravascular volume through hemorrhage,

you're in a you know a dire state and

we're going to try to want to replace

that. And usually what is in most

literature now supporting a 1:1 to1

ratio of packed red cells with uh FFP

and then also with platelets uh to make

sure that we're actually giving a

patient whole blood uh or kind of a a a

kind of construction of whole blood to

make sure that they're getting not just

oxygen carrying capacity but also clot

uh uh manufacturing capacity to make

sure that we can they can hypothetically

stop the bleeding that's going on. Now

somewhat related again I was kind of

alluding to the use of tranexemic acid

uh in certain scenarios and we actually

got a question related to this uh about

exactly how tranexemic acid is working

in this scenario. So uh tranexemic acid

is sometimes referred to as a

pro-coagulant in in reality it's

actually not a pro-coagulant. You

actually need to have an established

clot already formed with fibbrin

cross-linking. And what transmic acid is

actually doing is occupying a space uh

on the uh plasmine that's trying to

become activating and and deregulate

that fibbrin cross link. Uh it's going

into this lysine kind of binding

location that would normally exist where

the uh uh you know the fibbrin can link

with the plasmine and then degrade down

into a fibbrin degradation product. You

might have seen that on labs like a

d-dimer uh which is what would produce

so you're not going to be able to

stabilize a clot. You're not going to

have platelet cross linking anymore. So

what TXA is trying to do is occupy a

spot on the uh uh fibbrin molecule to

prevent the binding of uh the uh

plasmminogen to that site where uh

actually it's occupying the plasmin site

not the fibbrin site. So it's occupying

on the plasmine site and uh preventing

the the the binding of fibbrin to the

plasmminogen causing licis. So again

it's not to say that uh you know a a

caveat to that. The opposite effect is

something like tissue plasmin activator

which is actually going through that

process and allowing a plasmine or

plasminogen to be converted to plasma

and kind of licing that fibbrin cross

link that uh you've seen in many

textbooks and that's existing

physiologically. So that's kind of like

an induced coagalopathy that's going on.

But TXA is really just stabilizing the

existing fibbrin that's going on. And

what we can see from a lot of literature

is that um in this setting in massive

transfusion even in uh uh OB bleeding or

post hemorrhage bleeding uh after a

delivery in in in pregnant patients is

that we can hopefully stabilize a clot

by if there's an existing clot stabilize

it as much as possible by also giving

all these blood products uh and then

giving TXA can stabilize that even

further to try to hopefully resuscitate

resuscitate the patient. in many

literature settings we had actually seen

this uh occur from the crash uh trials

from the matter studies which are huge

landmark studies in these fields that

have kind of supported that. So again if

we're giving a massive transfusion two

of the key drugs that you should be

giving is uh TXA and support of that to

stabilize the existing clot and then

secondly one thing that often gets

overlooked uh is calcium. So you

probably learned in pharmacy school the

coagulation cascade and often most times

as faculty don't necessarily put where

calcium is absolutely necessary on that

cascade nor magnesium for that matter.

Uh but calcium is definitively necessary

to actually formulate and activate a lot

of these coagulation factors. So if we

are deficient in calcium or we can't uh

uh distribute it from other uh

hematologic storage sites like bone or

even the cycoplasmic reticulum to

actually occur in this setting, we

actually have to give it parentally. So

we're giving uh one to three grams of

calcium gluconate uh pretty readily with

this uh blood administration to make

sure we're actually forming a clot. So

hopefully I was able to answer that question.

question.

>> Yeah, Craig,

>> go ahead. We're at 7:25. So, why don't

we go ahead and take a a a quick break

here, guys. Um, so let give us about,

you know, six or seven minutes so you

guys can, you know, stand up, stretch,

get a drink, go to the restroom, and uh

we'll be we'll be right back. Okay,

Can you hear me? >> Yeah. Okay.

>> Yeah. Okay. Uh let's see.

Uh let's see. I think that's I think that was about

I think that's I think that was about six or seven minutes. So, um I would

six or seven minutes. So, um I would just go ahead and you know, for time

just go ahead and you know, for time sake, go ahead and keep going. And we'll

sake, go ahead and keep going. And we'll try to get to we'll get to your

try to get to we'll get to your questions,

questions, >> guys, uh towards the end. Um so, be

>> guys, uh towards the end. Um so, be patient. And if you have a question to

patient. And if you have a question to submit, go ahead and submit it and we'll

submit, go ahead and submit it and we'll do our best to answer it.

do our best to answer it. >> Sounds great. All right. So, uh, let's

>> Sounds great. All right. So, uh, let's keep going with open fractures. I know I

keep going with open fractures. I know I was kind of alluding to this early on,

was kind of alluding to this early on, but again, it's it's a it's a type of

but again, it's it's a it's a type of fracture of the bone tissue where

fracture of the bone tissue where essentially it's protruding through the

essentially it's protruding through the the skin layer. And depending on the the

the skin layer. And depending on the the the grade or the classification of it,

the grade or the classification of it, uh, we need to intervene from a pharmacy

uh, we need to intervene from a pharmacy standpoint in terms of antibiotic

standpoint in terms of antibiotic prophylaxis. the the size of the wound

prophylaxis. the the size of the wound that's going on is is dependent again on

that's going on is is dependent again on type one, two or three and almost always

type one, two or three and almost always we have to at least intervene on type

we have to at least intervene on type two or three open fractures with

two or three open fractures with spazzylin. Now as the escalates again up

spazzylin. Now as the escalates again up to higher grades of open fractures,

to higher grades of open fractures, we're going to have to add on other

we're going to have to add on other additional drug therapies typically a

additional drug therapies typically a amoglycide like gabapentin or not

amoglycide like gabapentin or not gabapentin genttoycin which is going to

gabapentin genttoycin which is going to be a key agent that we can utilize in

be a key agent that we can utilize in these scenarios. You a lot of this has

these scenarios. You a lot of this has to do with you know ongoing the patient

to do with you know ongoing the patient we're going to continue these uh until

we're going to continue these uh until and even afterwards they're with

and even afterwards they're with orthopedic surgery for uh surgical or

orthopedic surgery for uh surgical or non-surgical repair of that uh open

non-surgical repair of that uh open fracture. So after they reduce it again

fracture. So after they reduce it again we can uh continue it and hopefully uh

we can uh continue it and hopefully uh prevent any uh infection that was

prevent any uh infection that was otherwise going to occur in these

otherwise going to occur in these patients. Now with spinal cord injuries

patients. Now with spinal cord injuries related to trauma patients again these

related to trauma patients again these are uh quite dynamic injuries that go on

are uh quite dynamic injuries that go on with the patients uh that they can

with the patients uh that they can present in numerous different acute

present in numerous different acute settings but otherwise again it was

settings but otherwise again it was specific with the spinal cord area that

specific with the spinal cord area that has been injured is going to have quite

has been injured is going to have quite a myriad of presenting and neurological

a myriad of presenting and neurological issues uh from an acute care setting.

issues uh from an acute care setting. The drug therapy that we're really

The drug therapy that we're really looking at here is actually um you know

looking at here is actually um you know just trying to immobilize them and

just trying to immobilize them and stabilize them. There's a controversial

stabilize them. There's a controversial drug therapy with a very highdose

drug therapy with a very highdose corticosterative uh meloprenisolone

corticosterative uh meloprenisolone using up to 30 milligram per kilogram uh

using up to 30 milligram per kilogram uh for these patients. It's somewhat

for these patients. It's somewhat controversial in the literature. Uh and

controversial in the literature. Uh and we can go in very depth about that

we can go in very depth about that discussion too. But uh definitively a

discussion too. But uh definitively a lot of this has to do with treating the

lot of this has to do with treating the patient acute care surgically. They

patient acute care surgically. They could go into a neurogenic shock as

could go into a neurogenic shock as well. So kind of pertaining some of the

well. So kind of pertaining some of the clinical symptoms that are going on on

clinical symptoms that are going on on with that and manage them acutely in

with that and manage them acutely in that scenario. usually with vasopressors

that scenario. usually with vasopressors uh like phenylphrine uh not necessarily

uh like phenylphrine uh not necessarily norepinephrine early on but phenylphrine

norepinephrine early on but phenylphrine might actually support them in that

might actually support them in that setting uh and try to acutely manage

setting uh and try to acutely manage them but drug therapy with a spinal cord

them but drug therapy with a spinal cord injury again really has to do with that

injury again really has to do with that hemodynamic support and hypothetically

hemodynamic support and hypothetically extending it to uh corticosteroid

extending it to uh corticosteroid therapy but that really really really

therapy but that really really really definitively involves uh a lot of

definitively involves uh a lot of specialist involvement in acute care

specialist involvement in acute care surgery in in exactly what's going on

surgery in in exactly what's going on with these patients

with these patients >> yeah and from a board exam perspective I

>> yeah and from a board exam perspective I mean you're not going to see methyl

mean you're not going to see methyl predinis alone on the boards. It's a

predinis alone on the boards. It's a debated topic in clinical practice bias

debated topic in clinical practice bias by the neurosurgeons

by the neurosurgeons uh and their perspective or how what

uh and their perspective or how what level of functionality the patient had

level of functionality the patient had and what your ability is to maybe regain

and what your ability is to maybe regain something

something >> um of that. So it's but it's not a board

>> um of that. So it's but it's not a board question. It's just not going to be on

question. It's just not going to be on there because it's too too unre um

there because it's too too unre um unreliable. Go ahead. Right. So uh with

unreliable. Go ahead. Right. So uh with uh and in some of the other lectures I

uh and in some of the other lectures I know we kind of went in depth about uh

know we kind of went in depth about uh adult cardio life support so or ACLS in

adult cardio life support so or ACLS in resuscitation in numerous different

resuscitation in numerous different capacities but very briefly here with

capacities but very briefly here with pediatric patients. We actually have

pediatric patients. We actually have something called PALS or the pediatric

something called PALS or the pediatric advanced life support uh method. And a

advanced life support uh method. And a lot of the same things do overlap here

lot of the same things do overlap here with adult drug therapy and adult uh

with adult drug therapy and adult uh resuscitation. But there are some key

resuscitation. But there are some key differences just to reiterate with the

differences just to reiterate with the patient population being again pediatric

patient population being again pediatric where we actually will hypothetically

where we actually will hypothetically involve agents that aren't

involve agents that aren't hypothetically used anymore in adults in

hypothetically used anymore in adults in guideline settings like atropene in

guideline settings like atropene in these in these settings just from an

these in these settings just from an underlying knowledge of the different

underlying knowledge of the different physiologies and pathophysiologies that

physiologies and pathophysiologies that are relating to the cardiac arrest in

are relating to the cardiac arrest in these patients. So a lot of times it is

these patients. So a lot of times it is related to either a respiratory issue

related to either a respiratory issue like asthma or an aniflactoid reaction

like asthma or an aniflactoid reaction or perhaps trauma in that scenario also

or perhaps trauma in that scenario also but the drug therapy here does differ

but the drug therapy here does differ again just related to the atropene. Now

again just related to the atropene. Now uh doses aren't often you know focused

uh doses aren't often you know focused upon during uh many drug the or

upon during uh many drug the or pharmacologic or pharmacospety

pharmacologic or pharmacospety board exams but in this scenario I

board exams but in this scenario I actually attest that there could be some

actually attest that there could be some drug related and dosing related

drug related and dosing related questions just from the weight based

questions just from the weight based dosing perspective and the easiest way I

dosing perspective and the easiest way I remember it uh again it's just 0.02

remember it uh again it's just 0.02 milligram per kilogram for atropene and

milligram per kilogram for atropene and that's atine an easy way to remember

that's atine an easy way to remember that and you could extend that to

that and you could extend that to epinephrine which is 0.01 01 milligram

epinephrine which is 0.01 01 milligram per kilogram which you can actually

per kilogram which you can actually refer back to that aniflaxis uh dosing

refer back to that aniflaxis uh dosing regimen but again these are parental and

regimen but again these are parental and you can extend it to other drug

you can extend it to other drug therapies that we would see in adult in

therapies that we would see in adult in in adults if there's underlying abnormal

in adults if there's underlying abnormal rhythms like ventricular fibrillation or

rhythms like ventricular fibrillation or tacic cardia or if we've identified

tacic cardia or if we've identified uh causes of the arrest like

uh causes of the arrest like hypoglycemia we can give dextrose

hypoglycemia we can give dextrose usually D10 at least or up to D25 or D50

usually D10 at least or up to D25 or D50 depending on the age of the patient and

depending on the age of the patient and also sodium bicarbonate Again, not the

also sodium bicarbonate Again, not the 8.4% but usually a 4.2% which is a

8.4% but usually a 4.2% which is a little bit more uh likely not to cause

little bit more uh likely not to cause uh hemodynamic or vascular issues with

uh hemodynamic or vascular issues with the child that we're resuscitating. So a

the child that we're resuscitating. So a lot of that was related to a lot of

lot of that was related to a lot of acute care resuscitation and drug

acute care resuscitation and drug therapies. But we're going to take a

therapies. But we're going to take a evolution in this discussion to

evolution in this discussion to toxicology and talk about specific

toxicology and talk about specific agents and specific toxicology uh uh

agents and specific toxicology uh uh issues going on with them and how to

issues going on with them and how to manage these scenarios. So one of the

manage these scenarios. So one of the key ones, the first ones you actually

key ones, the first ones you actually see fairly often on board since there's

see fairly often on board since there's a lot you can actually test on in this

a lot you can actually test on in this capacity is acetaminophen or Tylenol

capacity is acetaminophen or Tylenol toxicity. Now the main metabolite here

toxicity. Now the main metabolite here that produces a toxic effect is napki or

that produces a toxic effect is napki or n acetto perobenzoquinonamine which is

n acetto perobenzoquinonamine which is actually produced by cychocchrome 21 uh

actually produced by cychocchrome 21 uh which can be induced in in in numerous

which can be induced in in in numerous capacities once we've exceeded our

capacities once we've exceeded our normal uh uh glucaronidation or

normal uh uh glucaronidation or sulfation capacity of normal

sulfation capacity of normal acetaminophen. So with this 211

acetaminophen. So with this 211 activation we can produce an excessive

activation we can produce an excessive amount of of nacki which can cause this

amount of of nacki which can cause this hpattoxicity in uh the uh kind of the

hpattoxicity in uh the uh kind of the tertiary region in the hpatocy. So in

tertiary region in the hpatocy. So in order to prevent this uh hpatotoxicity

order to prevent this uh hpatotoxicity and ultimately life-threatening injury

and ultimately life-threatening injury uh we're going to try to intervene as as

uh we're going to try to intervene as as soon as we can if we can administer

soon as we can if we can administer charcoal to a patient to try to prevent

charcoal to a patient to try to prevent any further absorption of the acino.

any further absorption of the acino. Obviously, we're going to do that in

Obviously, we're going to do that in almost any of these uh uh toxicology

almost any of these uh uh toxicology scenarios. But one of the key drug

scenarios. But one of the key drug therapies here that can definitely be

therapies here that can definitely be tested on is uh an acetylcysteine which

tested on is uh an acetylcysteine which is the I want to call it the antidote uh

is the I want to call it the antidote uh therapy for acetaminophen toxicity. Now

therapy for acetaminophen toxicity. Now it can be administered either in an IV

it can be administered either in an IV oral setting. So the IV dosing normally

oral setting. So the IV dosing normally the package insert or at least the

the package insert or at least the traditional dosing is a three drug or

traditional dosing is a three drug or three dose regimen where we give a

three dose regimen where we give a loading dose of 150 milligram per

loading dose of 150 milligram per kilogram followed by over one hour

kilogram followed by over one hour followed by 50 milligram per kilogram uh

followed by 50 milligram per kilogram uh IV over four hours and then uh 16

IV over four hours and then uh 16 milligram per kilogram uh that we're

milligram per kilogram uh that we're infusing over 16 hours and the easiest

infusing over 16 hours and the easiest way to remember the dosing in that

way to remember the dosing in that scenario because it it is a dosing

scenario because it it is a dosing scenario that might come up is the uh

scenario that might come up is the uh toxic dose level or the toxic level of

toxic dose level or the toxic level of an acid or sorry The toxic dose of an

an acid or sorry The toxic dose of an acettophen if you take it orally on a

acettophen if you take it orally on a weight based dose is about 150 milligram

weight based dose is about 150 milligram per kilogram. So the equivalent you can

per kilogram. So the equivalent you can relate that to the you know first dose

relate that to the you know first dose of an acetylcysteine IV which is 150

of an acetylcysteine IV which is 150 milligram per kilogram. Now there's an

milligram per kilogram. Now there's an alternative which is the oral route

alternative which is the oral route which is uh follows a similar loading

which is uh follows a similar loading dose than maintenance dose uh process

dose than maintenance dose uh process where you give 140 milligram per

where you give 140 milligram per kilogram orally for the patient and then

kilogram orally for the patient and then every four hours they get uh 70

every four hours they get uh 70 milligram per kilogram orally. Now if

milligram per kilogram orally. Now if you've ever been in a pharmacy and able

you've ever been in a pharmacy and able to smell or taste an acetylcysteine it

to smell or taste an acetylcysteine it is a rotten uh sulfurous smell and odor

is a rotten uh sulfurous smell and odor that tastes pretty terrible.

that tastes pretty terrible. So patients are going to have a hard

So patients are going to have a hard time tolerating it. um and almost always

time tolerating it. um and almost always vomit at least once through the drug

vomit at least once through the drug therapy. So it does involve some

therapy. So it does involve some complicated interventions. But just to

complicated interventions. But just to remember those are the two drug

remember those are the two drug therapies we will initiate for cetamidin

therapies we will initiate for cetamidin toxicity and usually continue it for at

toxicity and usually continue it for at least 20 hours before we can reassess uh

least 20 hours before we can reassess uh the tunnel level and whether the hpatocy

the tunnel level and whether the hpatocy uh hypatic enzymes as ALT have elevated

uh hypatic enzymes as ALT have elevated and we're going to also look at other

and we're going to also look at other parameters as well. So, uh,

parameters as well. So, uh, >> one real quick comment I would add on

>> one real quick comment I would add on there. One small question that you could

there. One small question that you could get is what to do. You know, how long do

get is what to do. You know, how long do you treat? So, Craig was providing you

you treat? So, Craig was providing you sort of the treatment recommendation,

sort of the treatment recommendation, but if there enzymes are still elevating

but if there enzymes are still elevating and you get towards the ends of the

and you get towards the ends of the regimen or it hasn't fully plateaued or

regimen or it hasn't fully plateaued or peaked yet, you might even continue it

peaked yet, you might even continue it beyond that. So, while it's a standard

beyond that. So, while it's a standard regimen, at some point, you may continue

regimen, at some point, you may continue to treat it, especially if they are

to treat it, especially if they are starting to improve clinically. Um, but

starting to improve clinically. Um, but I I don't know if they would ask I don't

I I don't know if they would ask I don't know if that it seemed like that would

know if that it seemed like that would come up to me because clinically you you

come up to me because clinically you you you you want to manage the patient.

you you want to manage the patient. You're not managing a number,

You're not managing a number, >> right? Absolutely.

>> right? Absolutely. >> Fundamentally.

>> Fundamentally. >> Absolutely. That's a excellent point. So

>> Absolutely. That's a excellent point. So with anticolinergic toxicity, I know it

with anticolinergic toxicity, I know it sounds like a kind of complex

sounds like a kind of complex terminology and we it's hard to relate

terminology and we it's hard to relate key drugs that involved with this, but

key drugs that involved with this, but actually one of the most common ones you

actually one of the most common ones you will see in clinical practice is dyen

will see in clinical practice is dyen hydramine uh exhibiting an antiolineric

hydramine uh exhibiting an antiolineric effect, especially not just in

effect, especially not just in therapeutic dosing, but in toxic dosing.

therapeutic dosing, but in toxic dosing. And the pneummonic in the presentation

And the pneummonic in the presentation that we see here is is almost kind of

that we see here is is almost kind of key in terms of remembering it. And the

key in terms of remembering it. And the the way that is often presented is as

the way that is often presented is as you can see here, the patient's going to

you can see here, the patient's going to present blind as a bat, dry as a bone.

present blind as a bat, dry as a bone. uh hot as a hair, mad as a hatter, and

uh hot as a hair, mad as a hatter, and red as a beat. Uh they they don't always

red as a beat. Uh they they don't always have all, you know, five of those

have all, you know, five of those different presentations, but if they

different presentations, but if they have at least one or two of those and

have at least one or two of those and you get good history, it's going to help

you get good history, it's going to help your uh determination of and narrowing

your uh determination of and narrowing your differential diagnosis, kind of

your differential diagnosis, kind of keying you in on what drug therapy you

keying you in on what drug therapy you can actually try or, you know,

can actually try or, you know, confirming other toxicologic exposures,

confirming other toxicologic exposures, other disease states that are going on.

other disease states that are going on. Um there's quite a lot you can also

Um there's quite a lot you can also extend upon with this pneummonic but we

extend upon with this pneummonic but we don't have to go into it but oddly it is

don't have to go into it but oddly it is specifically you're really just looking

specifically you're really just looking a lot of these key elements in the

a lot of these key elements in the patient presentation. Now these uh you

patient presentation. Now these uh you know it it the findings that you see

know it it the findings that you see here are almost kind of relating back to

here are almost kind of relating back to that pneummonic and a key example being

that pneummonic and a key example being the you know key antiolinergic and

the you know key antiolinergic and peripheral antiolin colonergic effects

peripheral antiolin colonergic effects where we're not having any secretion of

where we're not having any secretion of even uh you know uh you know uh

even uh you know uh you know uh hydration to your skin and tissues where

hydration to your skin and tissues where you're going to have no sweating

you're going to have no sweating available on the patient. So even if

available on the patient. So even if they're hypothermic, they're not going

they're hypothermic, they're not going to have any uh um you know any sweat

to have any uh um you know any sweat exposing on their tissue. So it's going

exposing on their tissue. So it's going to be something key you can look into

to be something key you can look into even in that scenario too. They're going

even in that scenario too. They're going to get a lot of uh redness in their skin

to get a lot of uh redness in their skin or in mucous membranes that you can try

or in mucous membranes that you can try and discern. Uh so a lot of these things

and discern. Uh so a lot of these things do kind of come into play when you're

do kind of come into play when you're trying to differentiate these patients

trying to differentiate these patients at least in an acute care setting. Now

at least in an acute care setting. Now the drug therapy here uh you can kind of

the drug therapy here uh you can kind of loop in a few different drug therapies.

loop in a few different drug therapies. uh but fiso stigmine is kind of the key

uh but fiso stigmine is kind of the key drug therapy that we would use in very

drug therapy that we would use in very specific scenarios. You don't use it in

specific scenarios. You don't use it in all anticolinergic toxicities but we do

all anticolinergic toxicities but we do use it in some and the way that it's

use it in some and the way that it's administered is you actually have to

administered is you actually have to administer kind of as a controlled bolus

administer kind of as a controlled bolus over about 10 minutes where we're giving

over about 10 minutes where we're giving anywhere from half to 1 milligram uh as

anywhere from half to 1 milligram uh as a slow infusion and the reason we're

a slow infusion and the reason we're doing it slowly is that we are trying to

doing it slowly is that we are trying to reverse the anticolinergic effects by

reverse the anticolinergic effects by giving aurgic agent. So if you give too

giving aurgic agent. So if you give too much of the fiso stigma or give it too

much of the fiso stigma or give it too rapidly, you're actually going to flip

rapidly, you're actually going to flip the patient from an antiolinergic

the patient from an antiolinergic toxicity into a colonergic toxicity

toxicity into a colonergic toxicity which actually we'll go in in a little

which actually we'll go in in a little bit uh a little bit later in one of the

bit uh a little bit later in one of the other uh slides. But in this you're

other uh slides. But in this you're actually just trying to look at whether

actually just trying to look at whether or not this is definitively almost like

or not this is definitively almost like a diagnostic aid that it is an

a diagnostic aid that it is an antiolinergic on board because otherwise

antiolinergic on board because otherwise we have no diagnostic definitive tests.

we have no diagnostic definitive tests. uh but it can help support that

uh but it can help support that diagnosis and then definitively figure

diagnosis and then definitively figure out what to do next. And usually it's

out what to do next. And usually it's just uh mental side support, airway

just uh mental side support, airway support, giving benzoazipines into

support, giving benzoazipines into support to make sure they're not

support to make sure they're not agitated and causing any secondary

agitated and causing any secondary injuries. So it's a complex drug therapy

injuries. So it's a complex drug therapy but um it is it can come up. Now aspirin

but um it is it can come up. Now aspirin and salicellate toxicity is somewhat uh

and salicellate toxicity is somewhat uh you know downregulated in terms of its

you know downregulated in terms of its prevalence fortunately uh but and we

prevalence fortunately uh but and we relate it to acetaminophen toxicity. But

relate it to acetaminophen toxicity. But the key difference here is with

the key difference here is with acetaminophen toxicity the the onset and

acetaminophen toxicity the the onset and hypothetical risk of uh mortality for

hypothetical risk of uh mortality for these patients is usually on the range

these patients is usually on the range of three to five days after the

of three to five days after the ingestion. But with uh aspirin and

ingestion. But with uh aspirin and salicellate ingestions the rate of

salicellate ingestions the rate of mortality is actually within the first

mortality is actually within the first day usually within 24 hours if not

day usually within 24 hours if not sooner after the the toxic ingestion. So

sooner after the the toxic ingestion. So this is actually a pretty potent and and

this is actually a pretty potent and and very terrifying agent to actually be

very terrifying agent to actually be exposed to on a toxicologic level. Um

exposed to on a toxicologic level. Um and ultimately what it does is it

and ultimately what it does is it uncouples oxidative phosphorilation. So

uncouples oxidative phosphorilation. So if you remember way back to your

if you remember way back to your biomedical or biochemistry classes after

biomedical or biochemistry classes after your KB cycle you tip into the oxidative

your KB cycle you tip into the oxidative phosphorilation and uh electron

phosphorilation and uh electron transport chain and essentially what

transport chain and essentially what aspirin does is it dis dissipates that

aspirin does is it dis dissipates that process where you can no longer generate

process where you can no longer generate ATP uh no matter what whether you're

ATP uh no matter what whether you're doing glycolysis whether you're doing

doing glycolysis whether you're doing lipolyis whether you're using protein in

lipolyis whether you're using protein in some amino acid generating process you

some amino acid generating process you just can't produce ATP anymore and your

just can't produce ATP anymore and your cells die almost very very rapidly now

cells die almost very very rapidly now in that setting aspirin The salicellate

in that setting aspirin The salicellate once it's absorbed can migrate from your

once it's absorbed can migrate from your peripheral circulation into your central

peripheral circulation into your central circulation uh and it affect your brain

circulation uh and it affect your brain tissue almost uh uh faster than it can

tissue almost uh uh faster than it can affect any other tissue largely from the

affect any other tissue largely from the pH differences you see in those

pH differences you see in those different compartments. So the way it

different compartments. So the way it gets trapped in there is is quite

gets trapped in there is is quite extensive. But the drug therapy we give

extensive. But the drug therapy we give here, so either GI decontamination, but

here, so either GI decontamination, but the sodium bicarbonate you see there is

the sodium bicarbonate you see there is actually related to actually trying to

actually related to actually trying to create a more alkaline environment in

create a more alkaline environment in your plasma to transit transmit that

your plasma to transit transmit that solicellate um uh product from your CNS

solicellate um uh product from your CNS back into your per peripheral

back into your per peripheral circulation and then hopefully get into

circulation and then hopefully get into uh your uh your kidney and your ur urine

uh your uh your kidney and your ur urine excretion because again the pH gets a

excretion because again the pH gets a little bit higher there. we can try to

little bit higher there. we can try to extrapolate that toxin out of your

extrapolate that toxin out of your system and prevent any further

system and prevent any further extrapolation of that impairment of

extrapolation of that impairment of oxidative phosphorilation in ATP

oxidative phosphorilation in ATP generation. So although it seems like a

generation. So although it seems like a supportive care in numerous other

supportive care in numerous other scenarios, the sodium bicarbonate is

scenarios, the sodium bicarbonate is almost definitive in in our management

almost definitive in in our management with these patients. So in in other

with these patients. So in in other patients that can't clear that uh uh

patients that can't clear that uh uh proton in the that salicellate from

proton in the that salicellate from their urine, we're definitely going to

their urine, we're definitely going to have to get on board and try to support

have to get on board and try to support them renally by getting them set up with

them renally by getting them set up with hemo hemodialysis to make sure that

hemo hemodialysis to make sure that things are ongoing. Now with the drug

things are ongoing. Now with the drug therapy related to this, obviously we're

therapy related to this, obviously we're giving a lot of sodium bicarbonate in

giving a lot of sodium bicarbonate in this setting. So one of the key adverse

this setting. So one of the key adverse events that does come up uh in many

events that does come up uh in many capacities is this hypoalemia that

capacities is this hypoalemia that you're going to induce by also giving

you're going to induce by also giving this high dose of sodium bicarbonate. So

this high dose of sodium bicarbonate. So something just to keep in mind and again

something just to keep in mind and again the again just to reiterate this is

the again just to reiterate this is actually a fairly high dosing. So not

actually a fairly high dosing. So not just again quoteunquote one unit of 50

just again quoteunquote one unit of 50 mill equivalents of sodium bicarbonate

mill equivalents of sodium bicarbonate but we're giving usually one milligram

but we're giving usually one milligram per kilog or one mill equivalent per

per kilog or one mill equivalent per kilogram and then titrating uh to a

kilogram and then titrating uh to a arterial pH of about 7.45. So that's

arterial pH of about 7.45. So that's that almost upper limit of a normal uh

that almost upper limit of a normal uh AG even almost to 7.5. uh we're getting

AG even almost to 7.5. uh we're getting the patients slightly alkalotic to make

the patients slightly alkalotic to make sure we're transitioning the solicate

sure we're transitioning the solicate out of the CNS into the plasma and then

out of the CNS into the plasma and then into urine and hopefully get these

into urine and hopefully get these patients a little bit better. But this

patients a little bit better. But this is a pretty complex uh uh toxicologic

is a pretty complex uh uh toxicologic scenario. Now with uh kind of looping

scenario. Now with uh kind of looping these two classes together, beta

these two classes together, beta blockers and calcium channel blockers

blockers and calcium channel blockers although they do have different effects

although they do have different effects uh from their pharmacologic standpoint

uh from their pharmacologic standpoint on what they're doing on different

on what they're doing on different receptors. So the beta blockers on

receptors. So the beta blockers on obviously the um atro sympathetic uh

obviously the um atro sympathetic uh neurotransmission and pathway into the

neurotransmission and pathway into the cardiac tissues and also other vascular

cardiac tissues and also other vascular tissues preventing epinephrine or

tissues preventing epinephrine or norepinephrine from binding to those

norepinephrine from binding to those receptors. uh calcium channel blockers

receptors. uh calcium channel blockers work also on a similar pathway but

work also on a similar pathway but somewhat different in that in that

somewhat different in that in that spectrum but off also I mean ultimately

spectrum but off also I mean ultimately what these agents are doing is trying to

what these agents are doing is trying to uh optimize calcium or prevent calcium

uh optimize calcium or prevent calcium communication and release within the

communication and release within the cell to activate muscle tissue and

cell to activate muscle tissue and contraction in different capacities even

contraction in different capacities even in cardiac conduction and also some

in cardiac conduction and also some other neural conductions as well. But in

other neural conductions as well. But in a toxicologic scenario, we kind of lump

a toxicologic scenario, we kind of lump both these together in in understanding

both these together in in understanding that again what we're trying to

that again what we're trying to accomplish is overcoming this calcium

accomplish is overcoming this calcium dependent calcium release from the

dependent calcium release from the psychoplastic reticulum where the

psychoplastic reticulum where the cardiac contractility and other

cardiac contractility and other contractility of other tissues has been

contractility of other tissues has been entirely compromised. So one of the ways

entirely compromised. So one of the ways we can actually do that is try to

we can actually do that is try to optimize the the release of calcium from

optimize the the release of calcium from these scenarios or bypass the uh uh

these scenarios or bypass the uh uh blockade of the beta the beta receptor

blockade of the beta the beta receptor by giving other agents. So starting with

by giving other agents. So starting with the beta blockers by bypassing the

the beta blockers by bypassing the blockade we can actually give glucagon

blockade we can actually give glucagon which can activate this secondarily to

which can activate this secondarily to get that calcium dependent calcium

get that calcium dependent calcium release going on through different

release going on through different mechanisms. So that's one agent we can

mechanisms. So that's one agent we can use. A dose is definitive in this

use. A dose is definitive in this scenario. So glucagon in a diabetic

scenario. So glucagon in a diabetic patient that's hypoglycemic we're giving

patient that's hypoglycemic we're giving about 1 milligram but in this scenario

about 1 milligram but in this scenario for toxicology we're giving anywhere

for toxicology we're giving anywhere from 2 to 10 milligrams. Um and related

from 2 to 10 milligrams. Um and related to that is definitely causing some

to that is definitely causing some nausea in these patients. But uh

nausea in these patients. But uh flipping to calcium channel blockers,

flipping to calcium channel blockers, some patients do get glucagon which

some patients do get glucagon which isn't necessarily effective in these

isn't necessarily effective in these scenarios. We actually defer to insulin

scenarios. We actually defer to insulin uh particularly highdosese insulin

uh particularly highdosese insulin therapy. So opposed to a 0.1 unit per

therapy. So opposed to a 0.1 unit per kilo which is what we would give to say

kilo which is what we would give to say a patient in DKA diabetic patient we're

a patient in DKA diabetic patient we're giving one unit per kilo. So this is 10

giving one unit per kilo. So this is 10 times more insulin which is quite a lot

times more insulin which is quite a lot of insulin. And what we're going to do

of insulin. And what we're going to do with the insulin again related to the

with the insulin again related to the insulin release and glucose absorption

insulin release and glucose absorption within the cell there's also also

within the cell there's also also calcium dependent entry into the cell

calcium dependent entry into the cell that we're trying to optimize in that

that we're trying to optimize in that scenario. So we're trying to optimize

scenario. So we're trying to optimize the calcium entry into the cell by

the calcium entry into the cell by giving this highdose insulin which is

giving this highdose insulin which is actually amplifying our ability to you

actually amplifying our ability to you know provide and and and provide cardiac

know provide and and and provide cardiac conduction and muscle contraction to

conduction and muscle contraction to overcome the uh you know card calcium

overcome the uh you know card calcium channel blocker effects that we normally

channel blocker effects that we normally see like bradic cardia and hypotension.

see like bradic cardia and hypotension. So a lot of these things are pretty key

So a lot of these things are pretty key with drug therapy, but again supportive

with drug therapy, but again supportive care with this. So with glucagon, we're

care with this. So with glucagon, we're going to have to treat the nausea

going to have to treat the nausea associated with it definitively. And

associated with it definitively. And with the highdosese insulin therapy,

with the highdosese insulin therapy, we're definitely going to have to manage

we're definitely going to have to manage the uh potential uh lowering of the

the uh potential uh lowering of the blood glucose. That can happen actually

blood glucose. That can happen actually quite quickly with these patients by

quite quickly with these patients by giving them supplemental glucose. And

giving them supplemental glucose. And again, the dose or the product of

again, the dose or the product of insulin we're using for this scenario is

insulin we're using for this scenario is insulin regular. But you can

insulin regular. But you can hypothetically use insulin aspart or

hypothetically use insulin aspart or lispro intravenously. That can be

lispro intravenously. That can be substituted. But we're either one is

substituted. But we're either one is going to be the same dose and somewhat

going to be the same dose and somewhat of the same concerns.

of the same concerns. So as I was kind of alluding to when I

So as I was kind of alluding to when I was talking about anticolinergic

was talking about anticolinergic toxicity uh where we might induce that

toxicity uh where we might induce that when we're giving uh you know fo stigma

when we're giving uh you know fo stigma to a patient that's anticolinergic with

to a patient that's anticolinergic with colonergic toxicity we can actually see

colonergic toxicity we can actually see some of the uh effects that we would

some of the uh effects that we would predict or want to try to screen for in

predict or want to try to screen for in that setting. And again we had that

that setting. And again we had that pneummonic with anticolinergic toxicity

pneummonic with anticolinergic toxicity but related to colonergic toxic

but related to colonergic toxic toxicity. There's a different pneummonic

toxicity. There's a different pneummonic uh which is the killer bees where we can

uh which is the killer bees where we can see broncharia bronco spasm and uh brada

see broncharia bronco spasm and uh brada cardardia occur in these patients. But

cardardia occur in these patients. But there's also another acronym that we do

there's also another acronym that we do recall for not necessarily as

recall for not necessarily as life-threatening adverse events uh from

life-threatening adverse events uh from colon colonergic agents like salivation,

colon colonergic agents like salivation, lacrimmation, urination, defecation, GI

lacrimmation, urination, defecation, GI distress and emmesis which stands for

distress and emmesis which stands for sludge. Uh but again killer bees is the

sludge. Uh but again killer bees is the one that we're really concerned with. So

one that we're really concerned with. So colonergic toxicity isn't as prevalent.

colonergic toxicity isn't as prevalent. We don't see it a lot uh in drug therapy

We don't see it a lot uh in drug therapy anymore fortunately but you can be you

anymore fortunately but you can be you can observe it in certain scenarios. Uh

can observe it in certain scenarios. Uh you know if a patient has an underlying

you know if a patient has an underlying psychiatric disease or if they have

psychiatric disease or if they have something like Parkinson's it might be

something like Parkinson's it might be on something that is optimizing uh

on something that is optimizing uh transmission. They are hypothetically at

transmission. They are hypothetically at risk for someone in that household being

risk for someone in that household being exposed to those drugs like a child uh

exposed to those drugs like a child uh could hypothetically be exposed to this.

could hypothetically be exposed to this. But in these scenarios again on a flip

But in these scenarios again on a flip from again what we were talking about

from again what we were talking about earlier with a colonergic toxicity we're

earlier with a colonergic toxicity we're trying to induce an anticolinergic agent

trying to induce an anticolinergic agent to try to reverse whatever is going on.

to try to reverse whatever is going on. So in this scenario we give atropene and

So in this scenario we give atropene and again fairly high doses of atropene but

again fairly high doses of atropene but we can also give other agents like

we can also give other agents like prowidoxim um and you might have heard

prowidoxim um and you might have heard of this as tupam uh and that's reserved

of this as tupam uh and that's reserved to for you know outpatient military use

to for you know outpatient military use uh or even you know uh human use or not

uh or even you know uh human use or not just necessarily human use but civilian

just necessarily human use but civilian use in certain scenarios but you largely

use in certain scenarios but you largely in the acute care setting we really only

in the acute care setting we really only care about atropene uh for a lot of

care about atropene uh for a lot of different uh reasons which I won't go

different uh reasons which I won't go into in too much depth here uh uh just

into in too much depth here uh uh just based on the the agent the toxin agent

based on the the agent the toxin agent that's being involved here.

that's being involved here. So dejoxin toxicity is somewhat unique

So dejoxin toxicity is somewhat unique that it it's quite an old agent we use

that it it's quite an old agent we use in cardiovascular uh management of

in cardiovascular uh management of certain patients. uh but we don't

certain patients. uh but we don't necessarily think it's going to be a

necessarily think it's going to be a prevalent toxin agent uh anymore but it

prevalent toxin agent uh anymore but it it truly has been in numerous capacities

it truly has been in numerous capacities either from the elderly patient or the

either from the elderly patient or the patient on the cardiac agent just

patient on the cardiac agent just ingesting it inappropriately or not

ingesting it inappropriately or not knowledgeably or a child in that

knowledgeably or a child in that household uh being exposed to it as

household uh being exposed to it as well. And these patients again it's

well. And these patients again it's somewhat related to our beta blocker and

somewhat related to our beta blocker and calcium channel blocker discussion where

calcium channel blocker discussion where we're looking at calcium dependent uh

we're looking at calcium dependent uh influx into the cell regulating calcium

influx into the cell regulating calcium dependent release that's ongoing for

dependent release that's ongoing for either conduction uh with these

either conduction uh with these electrical signals in the cardiac tissue

electrical signals in the cardiac tissue or in vascular tissue. So deoxin again

or in vascular tissue. So deoxin again working quite heavily in this pathway.

working quite heavily in this pathway. The only way we can actually try to

The only way we can actually try to reverse this is giving a a dejoxin

reverse this is giving a a dejoxin specific antidote by trying to bind it.

specific antidote by trying to bind it. And the only one available in the United

And the only one available in the United States nowadays is called Digifab. And

States nowadays is called Digifab. And it's a fragmented antibbody that's going

it's a fragmented antibbody that's going to bind up the available deoxin that's

to bind up the available deoxin that's free from tissues, but it's going to

free from tissues, but it's going to create this cascade where you're going

create this cascade where you're going to be able to uh deregulate and uh

to be able to uh deregulate and uh disassociate the deoxin from its

disassociate the deoxin from its therapeutic site into the plasma and

therapeutic site into the plasma and localize it there and eliminate it

localize it there and eliminate it definitively. Now, one of the key issues

definitively. Now, one of the key issues here to determine whether or not we're

here to determine whether or not we're going to give Digifab isn't necessarily

going to give Digifab isn't necessarily the Dejoxin level. It's actually the

the Dejoxin level. It's actually the potassium level in the patient. So if

potassium level in the patient. So if they're presenting with hypercalemia uh

they're presenting with hypercalemia uh usually even just slight hypercalemia

usually even just slight hypercalemia with a potassium slightly over the upper

with a potassium slightly over the upper therapeutic normal uh we're going to

therapeutic normal uh we're going to actually be in a in a realm where we're

actually be in a in a realm where we're going to hypothetically give djoxin

going to hypothetically give djoxin antidote so digifab if we can relate

antidote so digifab if we can relate whatever is going on with the patient

whatever is going on with the patient with a potential dioxin toxicity. So the

with a potential dioxin toxicity. So the the keys here is that you might not

the keys here is that you might not necessarily be driven to give digifab or

necessarily be driven to give digifab or treat a patient with digifab based on

treat a patient with digifab based on the digoxin level, but it's going to be

the digoxin level, but it's going to be more the the uh potassium level you're

more the the uh potassium level you're seeing in the patient acutely uh to

seeing in the patient acutely uh to determine what you're going to give. And

determine what you're going to give. And the dosing with digifab is dependent on

the dosing with digifab is dependent on the djoxin level. So that might be in

the djoxin level. So that might be in the question or in the clinical scenario

the question or in the clinical scenario to help you define what dose is going to

to help you define what dose is going to be appropriate. But uh determining its

be appropriate. But uh determining its drug therapy, you're looking largely at

drug therapy, you're looking largely at the potassium and hypothetically some

the potassium and hypothetically some other uh uh cardiac manifestations of

other uh uh cardiac manifestations of the deoxin toxicity.

the deoxin toxicity. Now with invenimations, it's quite a

Now with invenimations, it's quite a broad topic, but we can just loop it

broad topic, but we can just loop it into two broad categories that we see in

into two broad categories that we see in the United States, likely with a uh

the United States, likely with a uh North American pit viper, which is a

North American pit viper, which is a snake, or with some spiders. So with the

snake, or with some spiders. So with the North American pit vipers, uh we have

North American pit vipers, uh we have the eastern and western diamondbacks. We

the eastern and western diamondbacks. We have Mojave, we have uh pit uh uh

have Mojave, we have uh pit uh uh copperheads, we have uh water moccasins

copperheads, we have uh water moccasins or cotton mouths and quite a number of

or cotton mouths and quite a number of other uh native snakes in North America

other uh native snakes in North America that can cause quite a wide range of

that can cause quite a wide range of clinical symptoms. But say you have a

clinical symptoms. But say you have a patient present to the acute care

patient present to the acute care setting with a an obvious invenimation.

setting with a an obvious invenimation. We're going to quickly assess these

We're going to quickly assess these patients and oftent times almost defer

patients and oftent times almost defer uh to if they have a confirmation of an

uh to if they have a confirmation of an invenimation in systemic symptoms, we're

invenimation in systemic symptoms, we're going to give an antivenenom to try to

going to give an antivenenom to try to not necessarily reverse and we can't

not necessarily reverse and we can't necessarily reverse a lot of the tissue

necessarily reverse a lot of the tissue effects. Some of the hemodynamic and

effects. Some of the hemodynamic and coagulation effects that are occurring

coagulation effects that are occurring from Mojave or Western Diamondback, we

from Mojave or Western Diamondback, we can reverse. But in most patients like

can reverse. But in most patients like we see here in East Texas, even on the

we see here in East Texas, even on the eastern uh coast where we see a lot of

eastern uh coast where we see a lot of copperhead animations, we're going to

copperhead animations, we're going to stop the progression of tissue injury by

stop the progression of tissue injury by giving an antidote which is either uh uh

giving an antidote which is either uh uh anip or croab which are the brand names

anip or croab which are the brand names of the available snake antenoms North

of the available snake antenoms North American pit viper antvenenoms available

American pit viper antvenenoms available for us here in the United States. Now

for us here in the United States. Now depending which agent you give is

depending which agent you give is largely dependent on the formulary and

largely dependent on the formulary and almost uh always that we're not going to

almost uh always that we're not going to see a differentiation in determining and

see a differentiation in determining and being deciding which agent you have to

being deciding which agent you have to give on an exam. It's going to be one or

give on an exam. It's going to be one or the other. Um since both agents almost

the other. Um since both agents almost equivocally used uh for any North

equivocally used uh for any North American pit viper. Now flipping that

American pit viper. Now flipping that just very very briefly with spiders. We

just very very briefly with spiders. We have two main uh toxin producing uh

have two main uh toxin producing uh snake or spider species in the United

snake or spider species in the United States. So it's the uh cotton not cotton

States. So it's the uh cotton not cotton mouth the uh uh diamondback sorry not

mouth the uh uh diamondback sorry not the diamond back lubing all these snakes

the diamond back lubing all these snakes and spiders together is quite complex

and spiders together is quite complex but we have uh essentially two spher

but we have uh essentially two spher species in the United States that can

species in the United States that can cause some uh excessive pain uh uh

cause some uh excessive pain uh uh syndrome. So black widow is one that can

syndrome. So black widow is one that can cause excessive pain and maybe some

cause excessive pain and maybe some muscle spasms but usually isn't

muscle spasms but usually isn't life-threatening. There used to be an

life-threatening. There used to be an antidote available uh but it's largely

antidote available uh but it's largely no longer available. you might have to

no longer available. you might have to call a poison center to be involved with

call a poison center to be involved with it. Again, not going to be on the board

it. Again, not going to be on the board exam in this capacity. But we also have

exam in this capacity. But we also have a a brown recluse spider that can

a a brown recluse spider that can actually cause some coagulation

actually cause some coagulation abnormalities and some neurotoxicities

abnormalities and some neurotoxicities that hypothetically could need uh some

that hypothetically could need uh some antivenenom available. So again, there's

antivenenom available. So again, there's a lot of other species in the world that

a lot of other species in the world that can cause invenimations, but largely uh

can cause invenimations, but largely uh what we see in the United States is

what we see in the United States is largely just the spiders and the snakes.

largely just the spiders and the snakes. So malignant hypothermia is something

So malignant hypothermia is something you might see related to uh not

you might see related to uh not necessarily exposure to heat itself like

necessarily exposure to heat itself like fire or the sun but it could actually be

fire or the sun but it could actually be drug induced and one of the drugs we

drug induced and one of the drugs we actually talked about succoline is

actually talked about succoline is actually linked to malignant hypothermia

actually linked to malignant hypothermia and there's a lot of other uh sedative

and there's a lot of other uh sedative uh gases that are used in the O setting

uh gases that are used in the O setting that can cause malignant hypothermia as

that can cause malignant hypothermia as well and what this is related to is an

well and what this is related to is an excessive release of calcium from the

excessive release of calcium from the cycloplastic reticulum that I was kind

cycloplastic reticulum that I was kind of alluding to earlier by the specific

of alluding to earlier by the specific specific receptor, the rhinodine

specific receptor, the rhinodine receptor or R Y R1 receptor that gets uh

receptor or R Y R1 receptor that gets uh uh overly activated essentially uh and

uh overly activated essentially uh and it causes this extensive release of

it causes this extensive release of calcium where we have an excessive uh

calcium where we have an excessive uh muscle contraction causing hypothermia

muscle contraction causing hypothermia just from the accumulation of ATP and

just from the accumulation of ATP and utilization of it where we're looking at

utilization of it where we're looking at other methods of actually producing ATP

other methods of actually producing ATP um largely outside of uh normal uh

um largely outside of uh normal uh glucose metabolism, glucose uh

glucose metabolism, glucose uh consumption. So we're looking at other

consumption. So we're looking at other pathways that are essentially producing

pathways that are essentially producing quite a lot of heat and relating to the

quite a lot of heat and relating to the patient. So what we have to identify

patient. So what we have to identify these patients quite early on is whether

these patients quite early on is whether they get rigid uh before they become

they get rigid uh before they become hypothermic uh in the in in the drug

hypothermic uh in the in in the drug administration setting. So we can

administration setting. So we can identify the rigidity time it to a key

identify the rigidity time it to a key administration and have no other cause

administration and have no other cause for that muscle rigidity. We actually

for that muscle rigidity. We actually want to intervene quite quickly before

want to intervene quite quickly before they develop hypothermia because at that

they develop hypothermia because at that point it's going to be very difficult to

point it's going to be very difficult to treat the patient. uh and this could

treat the patient. uh and this could progress to rabdomiis uh vib and even uh

progress to rabdomiis uh vib and even uh disseminated intravascular

disseminated intravascular quagalopathies uh causing a lot of

quagalopathies uh causing a lot of hemorrhage in these patients um and

hemorrhage in these patients um and likely death

likely death uh if we can't reverse it early. So the

uh if we can't reverse it early. So the reversal agent is called dantrine and

reversal agent is called dantrine and what it's doing is kind of countering

what it's doing is kind of countering this if you could think of it although

this if you could think of it although it's not a calcium channel blocker uh I

it's not a calcium channel blocker uh I kind of relate it to that in a in an

kind of relate it to that in a in an action setting that is preventing the

action setting that is preventing the release of calcium from the cycloplasic

release of calcium from the cycloplasic reticulum. So it's almost counteracting

reticulum. So it's almost counteracting entirely what was going on uh as a drug

entirely what was going on uh as a drug induced cause for these agents. Now

induced cause for these agents. Now Dantrin is quite a large uh uh uh dose

Dantrin is quite a large uh uh uh dose of medication to be giving uh and you

of medication to be giving uh and you dose it based on the patient parameters

dose it based on the patient parameters and how severe their issue is but it

and how severe their issue is but it could be anywhere from five to even 50

could be anywhere from five to even 50 vials for the initial dose and there

vials for the initial dose and there different brands that provide different

different brands that provide different concentrations. So it can be quite

concentrations. So it can be quite extensive. Uh and as we're getting the

extensive. Uh and as we're getting the dantine, we're also going to want to use

dantine, we're also going to want to use some of the elements of uh intravascular

some of the elements of uh intravascular and extravascular cooling. Uh we can for

and extravascular cooling. Uh we can for these patients and again if we can relax

these patients and again if we can relax the patient as much as possible

the patient as much as possible releasing some of the muscle tension

releasing some of the muscle tension using benzodiaines we're going to try

using benzodiaines we're going to try that as well. Now medeanmia is something

that as well. Now medeanmia is something that we uh can see in in another drug

that we uh can see in in another drug induced setting uh in in many capacities

induced setting uh in in many capacities but we do see it from an outpatient

but we do see it from an outpatient setting as well. Now the the key here

setting as well. Now the the key here and you can kind of relate it to carbon

and you can kind of relate it to carbon monoxide exposure because it's somewhat

monoxide exposure because it's somewhat similar in the sense that we're

similar in the sense that we're preventing oxygen uh being released from

preventing oxygen uh being released from the hemoglobin molecule where in this

the hemoglobin molecule where in this state where it hasn't actually uh

state where it hasn't actually uh changed necessarily too dramatically but

changed necessarily too dramatically but instead of a F3 or an F2 ion or an ion 2

instead of a F3 or an F2 ion or an ion 2 molecule we in the hemoglobin we

molecule we in the hemoglobin we actually have an F3 uh creating an

actually have an F3 uh creating an affinity to the oxygen that's preventing

affinity to the oxygen that's preventing its release from the the hemoglobin

its release from the the hemoglobin molecule. We term this methemoglobin. So

molecule. We term this methemoglobin. So what we see in these patients presenting

what we see in these patients presenting that have been exposed to something

that have been exposed to something that's been causing this metmoglobin is

that's been causing this metmoglobin is a cyanotonic condition usually around

a cyanotonic condition usually around their lips or their mouth. It's going to

their lips or their mouth. It's going to be blue. It could be in other tissues

be blue. It could be in other tissues like their fingertips or their ears uh

like their fingertips or their ears uh becoming blue before they're you know

becoming blue before they're you know hemodynamically compromised. But it can

hemodynamically compromised. But it can progress to dysphonia uh feeling dizzy

progress to dysphonia uh feeling dizzy or fatigue ultramental status even

or fatigue ultramental status even arrhythmias and and presenting with uh

arrhythmias and and presenting with uh an entire entirely ultramental status.

an entire entirely ultramental status. And if we don't have any other

And if we don't have any other differential on the on the patient or we

differential on the on the patient or we can't necessarily identify anything else

can't necessarily identify anything else going on with that patient, we can

going on with that patient, we can measure the me hemoglobin by looking at

measure the me hemoglobin by looking at an arterial blood gas again. And if your

an arterial blood gas again. And if your lab doesn't necessarily include that on

lab doesn't necessarily include that on a in a on a normal AG, you can actually

a in a on a normal AG, you can actually request it be repeated or has already

request it be repeated or has already been done on that AG. You just have to

been done on that AG. You just have to request that information uh from the lab

request that information uh from the lab itself. And here again, most patients

itself. And here again, most patients can't normally be exposed to a high uh

can't normally be exposed to a high uh metoglobin level. Uh like again, if you

metoglobin level. Uh like again, if you smoked for example, it's going to be

smoked for example, it's going to be relatively normal. Uh so anything above

relatively normal. Uh so anything above 10% on that me hemoglobin is actually

10% on that me hemoglobin is actually going to defer us to uh how to treat

going to defer us to uh how to treat these patients quite acutely. And the

these patients quite acutely. And the treatment here is actually methylene

treatment here is actually methylene blue um and removing whatever agent is

blue um and removing whatever agent is involved. Now methylene blue is somewhat

involved. Now methylene blue is somewhat limited in that we have to make sure

limited in that we have to make sure it's the appropriate dose for these

it's the appropriate dose for these patients because if we overdose it in

patients because if we overdose it in this setting we actually induce meth

this setting we actually induce meth hemoglobin even further. So that can

hemoglobin even further. So that can hypothetically worsen it. So you don't

hypothetically worsen it. So you don't necessarily need to know the exact dose

necessarily need to know the exact dose of metmoglobin or methylene blue to

of metmoglobin or methylene blue to treat meth hemoglobinia. But you should

treat meth hemoglobinia. But you should uh keep in mind that if you're looking

uh keep in mind that if you're looking at a patient care scenario where they're

at a patient care scenario where they're getting methylene blue metalloglobin

getting methylene blue metalloglobin could actually become worse not

could actually become worse not necessarily better. Uh that's something

necessarily better. Uh that's something you might want to keep in mind. Now

you might want to keep in mind. Now neurolleptic malignant syndrome uh is

neurolleptic malignant syndrome uh is something we'll kind of relate to

something we'll kind of relate to serotonin syndrome which we'll have in a

serotonin syndrome which we'll have in a few slides in the future here but

few slides in the future here but neurolleptic malignant syndrome is

neurolleptic malignant syndrome is somewhat similar in the capacity that

somewhat similar in the capacity that you have a patient that is altered and

you have a patient that is altered and hypothermic. But some of the key

hypothermic. But some of the key differences between that and serotonin

differences between that and serotonin syndrome is a the onset of action or the

syndrome is a the onset of action or the onset of occurrence of neurolleptic

onset of occurrence of neurolleptic malignant syndrome which can actually

malignant syndrome which can actually happen in a quite delayed fashion um

happen in a quite delayed fashion um from days to weeks after the initiation

from days to weeks after the initiation of a drug therapy and it also has to do

of a drug therapy and it also has to do with different pathophysiology

with different pathophysiology specifically related to uh

specifically related to uh differentiation in dopamine transmission

differentiation in dopamine transmission uh within the CNS and this has to do

uh within the CNS and this has to do with a lot of uh antiscychotics and

with a lot of uh antiscychotics and anti-depressants that the patient may

anti-depressants that the patient may have been started on. So a lot of these

have been started on. So a lot of these issues lead to uh a lot of uh different

issues lead to uh a lot of uh different neur neurological signaling related to

neur neurological signaling related to uh dopamine specifically. And what we

uh dopamine specifically. And what we can see here is a tetratab syndrome. So

can see here is a tetratab syndrome. So we see a collection of this altermental

we see a collection of this altermental status, fever, muscle rigidity and

status, fever, muscle rigidity and autonomic dysfunction. And in numerous

autonomic dysfunction. And in numerous capacities, there's a lot of key

capacities, there's a lot of key symptoms here. Uh but just to relate

symptoms here. Uh but just to relate some of the muscle rigidity and

some of the muscle rigidity and autonomic dysfunction can relate to what

autonomic dysfunction can relate to what we call as cognial rigidity. So you have

we call as cognial rigidity. So you have a patient in a bed, you can hold up

a patient in a bed, you can hold up their arm and their arm is just going to

their arm and their arm is just going to stay there. And if you move it one

stay there. And if you move it one capacity, it'll just stay there in that

capacity, it'll just stay there in that same location and you keep moving it. Uh

same location and you keep moving it. Uh it's just going to stay in that uh

it's just going to stay in that uh capacity because their muscles are very

capacity because their muscles are very very rigid. It's tense and then it's not

very rigid. It's tense and then it's not going to have any capacity to actually

going to have any capacity to actually fall back down. Whereas if you have a

fall back down. Whereas if you have a patient, you're just assessing them and

patient, you're just assessing them and they're kind of uh mimicking some of

they're kind of uh mimicking some of these symptoms, you can hold it above uh

these symptoms, you can hold it above uh you know their body or some other

you know their body or some other capacity and as soon as you let go,

capacity and as soon as you let go, it'll fall back down. um and either

it'll fall back down. um and either might hit them or might not hit them

might hit them or might not hit them depending on the patient's mental

depending on the patient's mental status. Now, determining this is kind of

status. Now, determining this is kind of a collection of these identification of

a collection of these identification of these symptoms and also medication

these symptoms and also medication history before we can actually

history before we can actually definitively diagnose and and just kind

definitively diagnose and and just kind of uh differentially diagnose these

of uh differentially diagnose these patients uh in what's going on. And the

patients uh in what's going on. And the key drug therapy here is not just you

key drug therapy here is not just you know removing the causitive agent but

know removing the causitive agent but also trying to provide uh other agents

also trying to provide uh other agents like benzoazipines and bromeocryptine

like benzoazipines and bromeocryptine which actually can kind of try to

which actually can kind of try to augment the the transmission of the

augment the the transmission of the dopamine in these pathways to supersede

dopamine in these pathways to supersede the elimination of the of the drug

the elimination of the of the drug therapy which can be somewhat complex

therapy which can be somewhat complex especially in the days where we have

especially in the days where we have these depot injections of the

these depot injections of the antiscychotics like respperadone which

antiscychotics like respperadone which has been tied to this quite extensively.

has been tied to this quite extensively. Um uh and then again we'll kind of

Um uh and then again we'll kind of relate back when I go into serotonin

relate back when I go into serotonin toxicity but uh just to kind of relate

toxicity but uh just to kind of relate and some other key toxicities here uh

and some other key toxicities here uh opioid toxicity and uh before the

opioid toxicity and uh before the pandemic that we are all currently

pandemic that we are all currently living through with COVID uh opioid

living through with COVID uh opioid toxicity and opioid exposure was also

toxicity and opioid exposure was also somewhat considered as a pandemic in

somewhat considered as a pandemic in some capacities uh just from the overuse

some capacities uh just from the overuse of opioids in in our culture uh in

of opioids in in our culture uh in patients in outpatient settings and also

patients in outpatient settings and also patients just abusing them entirely. Uh

patients just abusing them entirely. Uh and the way we actually kind of

and the way we actually kind of stereotypically and kind of nor you know

stereotypically and kind of nor you know cognitively think about opioid toxicity

cognitively think about opioid toxicity is respiratory dysfunction. Um and one

is respiratory dysfunction. Um and one of the key issues here is that if a

of the key issues here is that if a patient administers their own opioid or

patient administers their own opioid or progressively administers their opioid

progressively administers their opioid uh they can get into the state where

uh they can get into the state where they actually don't respond uh

they actually don't respond uh appropriately to a hypoxic state. And

appropriately to a hypoxic state. And you can see this on their presentation

you can see this on their presentation where they have this um um hypoxia and

where they have this um um hypoxia and uh hypoxmia where they're not

uh hypoxmia where they're not necessarily breathing rapidly but

necessarily breathing rapidly but they're breathing very shallowly uh even

they're breathing very shallowly uh even though they're hypoxic on presentation

though they're hypoxic on presentation with an altermental status. So if you

with an altermental status. So if you can get a history from the patient or

can get a history from the patient or you can see any uh you know abuse marks

you can see any uh you know abuse marks of a parentally administered uh agent

of a parentally administered uh agent like a fentanyl which is on the on the

like a fentanyl which is on the on the black market now or heroin or if they're

black market now or heroin or if they're on a transermal fentanyl patch or

on a transermal fentanyl patch or they're just on extended release

they're just on extended release oxycodone as an oral agent any capacity

oxycodone as an oral agent any capacity of these if we can assess that and

of these if we can assess that and understand what's going on we can

understand what's going on we can empirically almost entirely empirically

empirically almost entirely empirically treat with nlloxxone uh which is the

treat with nlloxxone uh which is the opioid uh antagonist in this setting to

opioid uh antagonist in this setting to try to combat the receptor affinity And

try to combat the receptor affinity And essentially if we can see a neurologic

essentially if we can see a neurologic response or a response appropriate in

response or a response appropriate in this setting, we can actually continue

this setting, we can actually continue the nlloxxone also if it's in a uh an

the nlloxxone also if it's in a uh an extended release dosage form

extended release dosage form administration. So say they're on an

administration. So say they're on an oxycodone ER preparation, we can

oxycodone ER preparation, we can actually extend the infusion of

actually extend the infusion of nlloxxone to prevent the recurrence of

nlloxxone to prevent the recurrence of the opioid toxicity that's going on with

the opioid toxicity that's going on with any uh any of these patients. Um and

any uh any of these patients. Um and before I jump into sedative of hypnotic,

before I jump into sedative of hypnotic, Dr. Dr. Busai, did you have anything to

Dr. Dr. Busai, did you have anything to chime in on here at any of these uh

chime in on here at any of these uh topics I've been uh covering here?

topics I've been uh covering here? >> I mean, the from an opioid standpoint

>> I mean, the from an opioid standpoint that possibly could show up on the

that possibly could show up on the boards is, you know, the duration of

boards is, you know, the duration of action that you're going to get out of

action that you're going to get out of nlloxxone as you were pointing to with

nlloxxone as you were pointing to with some of the long acting is going to fall

some of the long acting is going to fall off. You got 45 minutes to maybe an

off. You got 45 minutes to maybe an hour, an hour and 15 minute window. It

hour, an hour and 15 minute window. It varies obviously for patient to patient,

varies obviously for patient to patient, but the if they have a long acting

but the if they have a long acting agent, you have to repeat the dose, then

agent, you have to repeat the dose, then you may even have to put them on a

you may even have to put them on a Narcan trip and and in that situation,

Narcan trip and and in that situation, you're admitting them to the hospital. I

you're admitting them to the hospital. I could see that potentially coming up

could see that potentially coming up >> um on a you know, boring. That's why we

>> um on a you know, boring. That's why we don't want to so quickly reverse

don't want to so quickly reverse somebody and then have them walk out of

somebody and then have them walk out of the emergency department all you know,

the emergency department all you know, pissed off. Um, and then as they're

pissed off. Um, and then as they're walking down the street, you know,

walking down the street, you know, cussing my name, they start to flow

cussing my name, they start to flow slowly

slowly go back down and then they show back up

go back down and then they show back up again. So, you know, we try to, you

again. So, you know, we try to, you know, balance that, but if they are

know, balance that, but if they are going to need a second dose, then you're

going to need a second dose, then you're probably concerned of a long acting

probably concerned of a long acting agent being uh present in the

agent being uh present in the background.

background. >> Yeah, absolutely. I mean, those are

>> Yeah, absolutely. I mean, those are excellent key points, not just for

excellent key points, not just for practice, but uh even on the board exam.

practice, but uh even on the board exam. Uh so coming back into the sedative

Uh so coming back into the sedative hypnotic toxicity. So we kind of alluded

hypnotic toxicity. So we kind of alluded to perhaps with some of the sedative

to perhaps with some of the sedative agents being benzodioizipines. Um but in

agents being benzodioizipines. Um but in this group we're actually kind of

this group we're actually kind of looping in uh three key classes here uh

looping in uh three key classes here uh of not just benzoizipines but

of not just benzoizipines but barbituates and also the

barbituates and also the non-benzoizipene

non-benzoizipene uh hypnotic agents like uh the sleep aid

uh hypnotic agents like uh the sleep aid agents like uh ambient or something like

agents like uh ambient or something like some of those agents that you might see

some of those agents that you might see being abused since they have a lot of

being abused since they have a lot of common pathways of uh action where

common pathways of uh action where they're acting on these GABA receptors

they're acting on these GABA receptors on your neurological pathways. Now uh

on your neurological pathways. Now uh again just not to dive into too deeply

again just not to dive into too deeply here but with bzzoizipines they actually

here but with bzzoizipines they actually uh activate and help the chloride

uh activate and help the chloride transmission through those uh pathways

transmission through those uh pathways in the presence of GABA. So you can

in the presence of GABA. So you can actually reach a a point where the

actually reach a a point where the patient can no longer you know you get

patient can no longer you know you get too toxic on the benzoazipene on its own

too toxic on the benzoazipene on its own since they require GABA which could be

since they require GABA which could be entirely depleted. So that chloride

entirely depleted. So that chloride transmission is actually shut down. Uh

transmission is actually shut down. Uh so they reach this sedative state which

so they reach this sedative state which isn't life-threatening. But with

isn't life-threatening. But with barbituates, you can actually extend

barbituates, you can actually extend that because it can work independent of

that because it can work independent of GABA by activating that chloride

GABA by activating that chloride receptor getting very um leading to

receptor getting very um leading to essentially seizure uh coma and death.

essentially seizure uh coma and death. And and if you read in in numerous

And and if you read in in numerous different capacities, it's actually used

different capacities, it's actually used in a lethal injection uh to cause uh CNS

in a lethal injection uh to cause uh CNS or brain death essentially. So we can

or brain death essentially. So we can extrapolate that to kind of a midground

extrapolate that to kind of a midground which is the non benzoazipines instead

which is the non benzoazipines instead of the sleep aids which are going to act

of the sleep aids which are going to act a little bit more like bzzoipines. But

a little bit more like bzzoipines. But if you have a scenario where a patient

if you have a scenario where a patient has co-ested something else, uh it's

has co-ested something else, uh it's going to extrapolate all those

going to extrapolate all those benzoazipene effects to be potentially

benzoazipene effects to be potentially life-threatening. So a lot of these uh

life-threatening. So a lot of these uh patients might present altered just a

patients might present altered just a little bit tired or even fully uh

little bit tired or even fully uh unconscious but still respirating

unconscious but still respirating appropriately but unable to arouse even

appropriately but unable to arouse even with painful stimuli. So they often get

with painful stimuli. So they often get uh intubated with an airway secure med

uh intubated with an airway secure med pretty quickly in that scenario. But

pretty quickly in that scenario. But after that it kind of deviates with what

after that it kind of deviates with what you might see in textbooks or even study

you might see in textbooks or even study references where it says consider

references where it says consider flammazinel. Now, flammazinil can be

flammazinel. Now, flammazinil can be used in certain uh toxicity settings

used in certain uh toxicity settings almost exclusively pediatrics uh or

almost exclusively pediatrics uh or patients that have never otherwise been

patients that have never otherwise been exposed to a benzoazipene largely

exposed to a benzoazipene largely because it's a it's essentially a a GABA

because it's a it's essentially a a GABA competitive antagonist. And the risk

competitive antagonist. And the risk here is that you can actually induce

here is that you can actually induce seizure activity uh from the fluinyl

seizure activity uh from the fluinyl itself which cannot be treated with

itself which cannot be treated with benzoazipines which you'd use to treat

benzoazipines which you'd use to treat the seizure. So you'd actually have to

the seizure. So you'd actually have to use uh other pathways, namely propal or

use uh other pathways, namely propal or ketamine could hypothetically work here,

ketamine could hypothetically work here, but it's actually a very difficult

but it's actually a very difficult seizure to treat. So you're really not

seizure to treat. So you're really not definitively going to use it in most

definitively going to use it in most patient settings. The patient settings

patient settings. The patient settings you are going to consider it if it's say

you are going to consider it if it's say again a a pediatric patient's never been

again a a pediatric patient's never been exposed to a benzoazipene, never expo

exposed to a benzoazipene, never expo been exposed to alcohol and took

been exposed to alcohol and took grandma's or their parents' medication

grandma's or their parents' medication accidentally or intentionally. Um that

accidentally or intentionally. Um that we could hypothetically reverse it

we could hypothetically reverse it before we get airway securement. um or

before we get airway securement. um or use it as a diagnostic aid almost where

use it as a diagnostic aid almost where we can give a micro dose of flumazinol

we can give a micro dose of flumazinol to see if there's a response uh before

to see if there's a response uh before we give a full dose or before we pro

we give a full dose or before we pro progress with um airway securement. So

progress with um airway securement. So one of the other uh hypothetical things

one of the other uh hypothetical things we could consider is sodium bicarbonate

we could consider is sodium bicarbonate and that's really for an inpatient

and that's really for an inpatient setting if a patient's been exposed to

setting if a patient's been exposed to more pheninoarbasol than they should

more pheninoarbasol than they should have just by creating an alkaline

have just by creating an alkaline environment to excrete it but that's

environment to excrete it but that's really exclusive just to phenobarbasol

really exclusive just to phenobarbasol not to all bzzoizipines. So that's just

not to all bzzoizipines. So that's just something to keep in mind. Um but again,

something to keep in mind. Um but again, yeah, go ahead Dr.

yeah, go ahead Dr. >> Busai. I think the other uh

>> Busai. I think the other uh >> uh realistic case scenario that you

>> uh realistic case scenario that you could see where from um is used is in a

could see where from um is used is in a procedural sedation. So

procedural sedation. So >> Oh yeah, absolutely.

>> Oh yeah, absolutely. >> I've done procedures in the emergency

>> I've done procedures in the emergency department. I've given you know patients

department. I've given you know patients uh what what is appropriate amount of

uh what what is appropriate amount of versed or something and I fixed the

versed or something and I fixed the scenario but it turns out that the

scenario but it turns out that the versed was a little too much and you

versed was a little too much and you know that's an appropriate situation

know that's an appropriate situation where I induced it and they have no

where I induced it and they have no history of benzodazipene use. You can

history of benzodazipene use. You can use uh fazinol in that situation to

use uh fazinol in that situation to reverse them. No different than the

reverse them. No different than the pediatric patient who accidentally

pediatric patient who accidentally swallows you know pills that they've

swallows you know pills that they've never taken before and it won't cause

never taken before and it won't cause withdrawal seizures.

withdrawal seizures. >> That's a great point. Absolutely. So

>> That's a great point. Absolutely. So again jumping back to neurolleptic

again jumping back to neurolleptic malignant syndrome or NMS uh again

malignant syndrome or NMS uh again relating to serotonin syndrome. So NMS

relating to serotonin syndrome. So NMS again I I mentioned it it occurs and we

again I I mentioned it it occurs and we can kind of overlap these things but

can kind of overlap these things but occurs kind of delayed fashion. So a day

occurs kind of delayed fashion. So a day or a couple days after the agent's been

or a couple days after the agent's been exposed to the patient but with

exposed to the patient but with serotonin syndrome uh it it occurs

serotonin syndrome uh it it occurs actually quite rapidly almost within an

actually quite rapidly almost within an hour even sometimes minutes from

hour even sometimes minutes from exposure of the serotonin agent uh the

exposure of the serotonin agent uh the patient has either ingested or smoked or

patient has either ingested or smoked or or consumed otherwise. So, and again a

or consumed otherwise. So, and again a departure from this uh again not

departure from this uh again not relating too much back to NMS but this

relating too much back to NMS but this here again as the name implies is an

here again as the name implies is an excess serotonin an excessive

excess serotonin an excessive stimulation of serotonin receptors in

stimulation of serotonin receptors in our uh neurologic pathways in other

our uh neurologic pathways in other different pathways as well but largely

different pathways as well but largely neurologic which leads to quite a lot of

neurologic which leads to quite a lot of different symptoms largely uh related to

different symptoms largely uh related to alternal status but you also get this

alternal status but you also get this mitriasis which can occur quite early on

mitriasis which can occur quite early on but hyper reflexia clonus and

but hyper reflexia clonus and diapharesis and there's a lot of other

diapharesis and there's a lot of other kind of complex of symptoms you can see

kind of complex of symptoms you can see in a patient where they're just so

in a patient where they're just so rigid, uh, very hyperothermic,

rigid, uh, very hyperothermic, hyperrelexive. um where even the lower

hyperrelexive. um where even the lower extremity again even as a pharmacist if

extremity again even as a pharmacist if you're in that capacity you can actually

you're in that capacity you can actually you know aid in this and perceive it

you know aid in this and perceive it where you're hyperflexating either the

where you're hyperflexating either the the the lower extremity um either the

the the lower extremity um either the foot and just seeing some clonus develop

foot and just seeing some clonus develop from that or even the lower extremity on

from that or even the lower extremity on the knee where you could stimulate the

the knee where you could stimulate the uh uh the the neurologic knee reflex and

uh uh the the neurologic knee reflex and actually see uh clonus occur in that

actually see uh clonus occur in that lower extremity before anything else

lower extremity before anything else happens in upper extremities. So, it's

happens in upper extremities. So, it's something actually quite definitive you

something actually quite definitive you can see on these serotonin serotonin

can see on these serotonin serotonin syndrome patients. Um, and again,

syndrome patients. Um, and again, another easy one is just taking a

another easy one is just taking a temperature. They're almost always going

temperature. They're almost always going to be hypothermic. Um, and there's

to be hypothermic. Um, and there's definitive diagnostic criteria, but

definitive diagnostic criteria, but oftentimes in the acute care setting,

oftentimes in the acute care setting, we're seeing these symptoms with a

we're seeing these symptoms with a patient history either with a a new drug

patient history either with a a new drug therapy or something exposed to them

therapy or something exposed to them that were kind of coming into play with

that were kind of coming into play with the history and incorporating all these

the history and incorporating all these symptoms that we're seeing and almost

symptoms that we're seeing and almost kind of going along with this could

kind of going along with this could hypothetically be serotonin syndrome.

hypothetically be serotonin syndrome. And one of the things we do here, again,

And one of the things we do here, again, it doesn't sound like a, you know, crazy

it doesn't sound like a, you know, crazy drug therapy or novel, but we give a

drug therapy or novel, but we give a highdose benzoazipene largely to try to

highdose benzoazipene largely to try to provide muscle relaxation to try to

provide muscle relaxation to try to counteract the serotonin serotonin

counteract the serotonin serotonin neurologic effects on the muscle tissue

neurologic effects on the muscle tissue by just trying to relax the muscle

by just trying to relax the muscle tissue uh using a highdose bzzodiz uh

tissue uh using a highdose bzzodiz uh and and try to counteract that. But in

and and try to counteract that. But in certain mild to moderate cases of

certain mild to moderate cases of serotonin syndrome that aren't

serotonin syndrome that aren't necessarily life-threatening, you could

necessarily life-threatening, you could give something like cypraepadine uh

give something like cypraepadine uh which can be used uh quite rapidly in in

which can be used uh quite rapidly in in certain clinical scenarios to try to

certain clinical scenarios to try to overcome this some of the serotonin

overcome this some of the serotonin effects. Uh but again it's it's somewhat

effects. Uh but again it's it's somewhat listed on the boards and other

listed on the boards and other references in very severe cases but

references in very severe cases but almost you would never use it without a

almost you would never use it without a benzoazipene on board. Um and this is

benzoazipene on board. Um and this is another scenario where um similar to

another scenario where um similar to alcohol withdrawal which we might go

alcohol withdrawal which we might go into a little bit later where the the

into a little bit later where the the core context with benzoipines we

core context with benzoipines we actually uh think about in numerous

actually uh think about in numerous different settings where we don't want

different settings where we don't want one that's long acting. We don't want

one that's long acting. We don't want one with active metabolites uh because

one with active metabolites uh because of prolonged duration of effect. But in

of prolonged duration of effect. But in this scenario we actually do want that.

this scenario we actually do want that. We do want a long acting benzodizopene

We do want a long acting benzodizopene with multiple active metabolites because

with multiple active metabolites because what we'll actually get is a better

what we'll actually get is a better control of the patient by giving early

control of the patient by giving early high doses and not necessarily have to

high doses and not necessarily have to give repetitive doses. So the key agent

give repetitive doses. So the key agent here that we use is dasopam which has

here that we use is dasopam which has numerous uh active metabolites opposed

numerous uh active metabolites opposed to laoropam which is a water- soluble

to laoropam which is a water- soluble benzoazipene which actually has

benzoazipene which actually has glucaronidation through his metabolism.

glucaronidation through his metabolism. Sorry not water soluble just

Sorry not water soluble just glucaronidation not oxidation uh where

glucaronidation not oxidation uh where it can be metabolized definitively in

it can be metabolized definitively in those patients but again we're lacking

those patients but again we're lacking that active metabolite that's going to

that active metabolite that's going to prolong its duration effect. So we just

prolong its duration effect. So we just have to dose it rapidly and those

have to dose it rapidly and those patients do kind of get overlooked uh in

patients do kind of get overlooked uh in different scenarios. So it that could be

different scenarios. So it that could be a test question that could come up just

a test question that could come up just saying that uh daipopane was actually

saying that uh daipopane was actually preferred uh in this patient scenario.

preferred uh in this patient scenario. Now uh sympathomimedic

Now uh sympathomimedic toxicity can actually present somewhat

toxicity can actually present somewhat similar to serotonin toxicity in the

similar to serotonin toxicity in the sense that the patients present somewhat

sense that the patients present somewhat agitated but very hyperothermic very uh

agitated but very hyperothermic very uh diaphoritic uh very red uh again if

diaphoritic uh very red uh again if they're not on a beta blocker they're

they're not on a beta blocker they're not going to be diaphoretic or not be

not going to be diaphoretic or not be takart necessarily could be di

takart necessarily could be di diaphoritic but uh we're going to make

diaphoritic but uh we're going to make sure that we can actually identify these

sure that we can actually identify these patients pretty rapidly and the

patients pretty rapidly and the sympathomimedic we're actually talking a

sympathomimedic we're actually talking a lot about here we can allude to in a

lot about here we can allude to in a little bit more depth later on um with

little bit more depth later on um with cocaine But also some other agents we

cocaine But also some other agents we we've talked about before with the uh

we've talked about before with the uh the methylmphetamines can also kind of

the methylmphetamines can also kind of lump into this as well where you just

lump into this as well where you just see a very uh tacocartic hyperactive

see a very uh tacocartic hyperactive patient uh very uh hyperothermic

patient uh very uh hyperothermic potentially with hyper attacki in every

potentially with hyper attacki in every capacity you can set assess on a

capacity you can set assess on a physical exam or uh uh different lab

physical exam or uh uh different lab settings as well. uh and we can see some

settings as well. uh and we can see some physiologic manifestations that are

physiologic manifestations that are potentially harmful to these patients

potentially harmful to these patients with all this excited state in the uh

with all this excited state in the uh neurologic dis uh discharge from their

neurologic dis uh discharge from their CNS. Uh we can see some hypoxia in the

CNS. Uh we can see some hypoxia in the tissues develop just from this over

tissues develop just from this over stimulation without appropriate oxygen

stimulation without appropriate oxygen delivery or glycolysis that's going on

delivery or glycolysis that's going on that can lead to metabolic acidosis and

that can lead to metabolic acidosis and ultimately endorgan dysfunction. Um and

ultimately endorgan dysfunction. Um and although again there's a complex

although again there's a complex pathophysiology going on here, the drug

pathophysiology going on here, the drug therapy involved with treating this is

therapy involved with treating this is actually very very simple. Again, we're

actually very very simple. Again, we're giving benzoizipines again at a very

giving benzoizipines again at a very high dose early on, not necessarily

high dose early on, not necessarily worrying about their airway compromise,

worrying about their airway compromise, but really trying to treat them

but really trying to treat them aggressively to try to mitigate some of

aggressively to try to mitigate some of these hyperactive components going on

these hyperactive components going on and if we can try to reverse the agent

and if we can try to reverse the agent otherwise if we can specifically

otherwise if we can specifically identify it. Now, we've been talking a

identify it. Now, we've been talking a lot about toxicities, but there's also

lot about toxicities, but there's also some withdrawal symptoms we can occur in

some withdrawal symptoms we can occur in observe in clinical scenarios that we do

observe in clinical scenarios that we do need to intervene on related to some of

need to intervene on related to some of these agents. So alcohol withdrawal is

these agents. So alcohol withdrawal is something you've probably been exposed

something you've probably been exposed to in numerous capacities in the sense

to in numerous capacities in the sense that uh with alcohol chronic consumption

that uh with alcohol chronic consumption we actually downregulate a a lot of

we actually downregulate a a lot of these GABA receptors uh where if we no

these GABA receptors uh where if we no longer expose ourselves or that the

longer expose ourselves or that the patient no longer exposes themselves to

patient no longer exposes themselves to alcohol we have a deficiency of GABA

alcohol we have a deficiency of GABA receptors where uh the patient can

receptors where uh the patient can actually become a little bit uh you know

actually become a little bit uh you know uh hyperactive in in in terms of their

uh hyperactive in in in terms of their CNS capacity where we get this

CNS capacity where we get this excitability and psychrometer agitation.

excitability and psychrometer agitation. related to the physiology that they've

related to the physiology that they've encountered from that chronic alcohol

encountered from that chronic alcohol consumption. So clinically we can see

consumption. So clinically we can see this in patients presenting with these

this in patients presenting with these hallucinations or uh these delirium

hallucinations or uh these delirium visions or delirium issues uh or

visions or delirium issues uh or altermet and seizures entirely. And uh

altermet and seizures entirely. And uh ultimately the way we try to intervene

ultimately the way we try to intervene on this is overcoming the uh

on this is overcoming the uh downregulation of GABA receptors by just

downregulation of GABA receptors by just giving GABA stimulating agents again

giving GABA stimulating agents again like benzodiaines. In some scenarios, we

like benzodiaines. In some scenarios, we actually like um uh phenobarbatital in

actually like um uh phenobarbatital in this scenario or barbbituous

this scenario or barbbituous specifically because if we have a

specifically because if we have a deficiency in GABA itself, the

deficiency in GABA itself, the benzoipene isn't going to work very

benzoipene isn't going to work very effectively. But we can use barbituates

effectively. But we can use barbituates again in independent of GABA to activate

again in independent of GABA to activate that chloride receptor and we can almost

that chloride receptor and we can almost always help improve these patients. Now

always help improve these patients. Now it's different dosing than you would see

it's different dosing than you would see in something like a a seizure disorder

in something like a a seizure disorder and almost especially since the

and almost especially since the patient's been exposed to a benzoazipene

patient's been exposed to a benzoazipene also but we can give a low fixed dose of

also but we can give a low fixed dose of a pheninoarbatital for these patients

a pheninoarbatital for these patients and actually help them improve. Now if

and actually help them improve. Now if they're not needing directed therapy

they're not needing directed therapy acutely we also have to prevent these uh

acutely we also have to prevent these uh progression of uh CNS excitation leading

progression of uh CNS excitation leading to something called delirium tremens by

to something called delirium tremens by giving uh low fixed doses of

giving uh low fixed doses of benzoizipines in a controlled setting

benzoizipines in a controlled setting following a number of different

following a number of different protocols and largely the SIA protocol

protocols and largely the SIA protocol is what you see commonly in clinical

is what you see commonly in clinical practice. Now, one clinical pearl here

practice. Now, one clinical pearl here and that might come up on an exam is

and that might come up on an exam is that in the critical care setting, the

that in the critical care setting, the SEA score hasn't necessarily been

SEA score hasn't necessarily been validated to the point where you can use

validated to the point where you can use it in that setting. So, although we use

it in that setting. So, although we use it clinically in numerous capacities, in

it clinically in numerous capacities, in that setting, it hasn't been

that setting, it hasn't been definitively validated. So, that might

definitively validated. So, that might come up on on a board exam in that

come up on on a board exam in that capacity. Now bofphen is an agent we

capacity. Now bofphen is an agent we sometime loop into benzoizipines in in

sometime loop into benzoizipines in in terms of its pharmacologic action

terms of its pharmacologic action clinically but there is a quite uh uh

clinically but there is a quite uh uh notable differentiation in its

notable differentiation in its pharmacologic mechanism in that although

pharmacologic mechanism in that although it acts on a gaba receptor it's actually

it acts on a gaba receptor it's actually the gaba b receptor uh which blephin

the gaba b receptor uh which blephin works on where bzzodizipines and

works on where bzzodizipines and barbbiters work on gaba a now the

barbbiters work on gaba a now the difference here with gaba b and backfin

difference here with gaba b and backfin withdrawal is you can have both a

withdrawal is you can have both a complex of uh ex uh kind kind of like an

complex of uh ex uh kind kind of like an excitation and inhibition going on at

excitation and inhibition going on at the same time where this decrease in

the same time where this decrease in GABA activity can actually lead to a

GABA activity can actually lead to a stimulation of alpha and gamma mediated

stimulation of alpha and gamma mediated skeletal muscle activity. So you could

skeletal muscle activity. So you could actually either see a patient that is

actually either see a patient that is totally weak, almost paralyzed and not

totally weak, almost paralyzed and not respirating appropriately to a patient

respirating appropriately to a patient that's uh kind of uh manifesting seizure

that's uh kind of uh manifesting seizure activity or CNS excitation. And it kind

activity or CNS excitation. And it kind of differentiates depending on on the

of differentiates depending on on the patient in different scenarios. In

patient in different scenarios. In different clinical scenarios, you might

different clinical scenarios, you might see where a patient isn't necessarily on

see where a patient isn't necessarily on chronic uh oral blephin use, but is on a

chronic uh oral blephin use, but is on a subcutaneous pump where there has been a

subcutaneous pump where there has been a malfunction in the pump or the the

malfunction in the pump or the the reservoir of the pump has been depleted

reservoir of the pump has been depleted that hasn't been resolved and the

that hasn't been resolved and the patients now seeming like they're

patients now seeming like they're overdosing on backin but is actually

overdosing on backin but is actually withdrawing. Now, if you can identify

withdrawing. Now, if you can identify these patients, again, the drug therapy

these patients, again, the drug therapy isn't uh very uh landmark here. It's

isn't uh very uh landmark here. It's benzoipines. you're just trying to

benzoipines. you're just trying to supplement GABA activity, not

supplement GABA activity, not necessarily overcoming the GABA B uh

necessarily overcoming the GABA B uh agents. You're just using GABA A in the

agents. You're just using GABA A in the setting to overcome the intracellular

setting to overcome the intracellular effects that the GABA receptors are

effects that the GABA receptors are having. But we can utilize the the

having. But we can utilize the the benzoizipines as much as possible until

benzoizipines as much as possible until we can reinitiate backin in these

we can reinitiate backin in these patients.

patients. Now, kind of alluding to all these

Now, kind of alluding to all these benzoazipines we're using in these

benzoazipines we're using in these different clinical scenarios, uh if we

different clinical scenarios, uh if we don't continue the therapy or titrate

don't continue the therapy or titrate them off appropriately, we can actually

them off appropriately, we can actually cause a withdrawal. And the withdrawal

cause a withdrawal. And the withdrawal you actually see from bzzoipene is

you actually see from bzzoipene is almost analogous to an alcohol

almost analogous to an alcohol withdrawal symptom or syndrome that

withdrawal symptom or syndrome that we're seeing. So a lot of the same

we're seeing. So a lot of the same symptoms can occur. The same

symptoms can occur. The same pathophysiology almost identically can

pathophysiology almost identically can occur and the same drug therapy can

occur and the same drug therapy can occur where we're just trying to replace

occur where we're just trying to replace the bzzoipines that the patient might be

the bzzoipines that the patient might be withdrawing from. Now afterwards once

withdrawing from. Now afterwards once we've been able to do that

we've been able to do that therapeutically and get them titrated

therapeutically and get them titrated down in a controlled fashion they're

down in a controlled fashion they're definitely going to need some

definitely going to need some psychiatric care to identify exactly why

psychiatric care to identify exactly why they're on a you know or medical therapy

they're on a you know or medical therapy to identify why they're on a chronic

to identify why they're on a chronic benzoazipene which led to a

benzoazipene which led to a discontinuation or an abruption in their

discontinuation or an abruption in their drug therapy and try to intervene where

drug therapy and try to intervene where we can prevent that from happening again

we can prevent that from happening again uh to kind of get into this clinical

uh to kind of get into this clinical scenario.

scenario. Now again we're alluding to and talking

Now again we're alluding to and talking a lot about opioid toxicity in that

a lot about opioid toxicity in that setting and and where we're using the

setting and and where we're using the lock zone but opioids can actually cause

lock zone but opioids can actually cause some opioid withdrawal as well. Now the

some opioid withdrawal as well. Now the differentiation here which is a large

differentiation here which is a large differentiation between alcohol or

differentiation between alcohol or benzodizopene withdrawal is that opioid

benzodizopene withdrawal is that opioid withdrawal in and of itself on its own

withdrawal in and of itself on its own is actually not toxic or not lethal

is actually not toxic or not lethal necessarily. So there is a a ve a very

necessarily. So there is a a ve a very old movie I always use to teach my

old movie I always use to teach my residents about this called Train

residents about this called Train Spotting and a very famous actor who

Spotting and a very famous actor who plays Obi-Wan uh nowadays uh actually

plays Obi-Wan uh nowadays uh actually was initially starring in that movie but

was initially starring in that movie but you can actually see him go through his

you can actually see him go through his opio withdrawal in a very clinically

opio withdrawal in a very clinically accurate setting uh in a in a film

accurate setting uh in a in a film setting also. Um but the key here that

setting also. Um but the key here that I'm trying to uh allude to is that

I'm trying to uh allude to is that opioid withdrawal in and of itself is

opioid withdrawal in and of itself is not life-threatening. a patient is going

not life-threatening. a patient is going to be very very discomforted uh going

to be very very discomforted uh going through a lot of uh physiological and

through a lot of uh physiological and psychiatric issues but which are very

psychiatric issues but which are very traumatic psychologically but in and of

traumatic psychologically but in and of itself isn't fatal. So we can support

itself isn't fatal. So we can support the patient uh symptomatically try to

the patient uh symptomatically try to support a lot of these symptoms uh as

support a lot of these symptoms uh as they go through withdrawal but not

they go through withdrawal but not necessarily abrupt the the withdrawal uh

necessarily abrupt the the withdrawal uh so they can get to the therapeutic

so they can get to the therapeutic endpoint of being free of the opioid

endpoint of being free of the opioid dependent uh nature that they're

dependent uh nature that they're physiologically adapted to from its

physiologically adapted to from its abuse and then they can transition um to

abuse and then they can transition um to something like a buprenorphine with or

something like a buprenorphine with or without nlloxxone or a methadone uh if

without nlloxxone or a methadone uh if they have kind of gotten halfway um or

they have kind of gotten halfway um or even fully and we need to prevent them

even fully and we need to prevent them from going back into an opioid toxic

from going back into an opioid toxic scenario um and it it's something that

scenario um and it it's something that is is quite complex but again you do

is is quite complex but again you do want to uh uh treat those

want to uh uh treat those symptomatically. Now there is a caveat

symptomatically. Now there is a caveat here that if they are withdrawing with

here that if they are withdrawing with uh you know something like an alcohol

uh you know something like an alcohol withdrawal on top of that you do

withdrawal on top of that you do definitely need to treat them

definitely need to treat them empirically uh because it could be

empirically uh because it could be hypothetically life-threatening or

hypothetically life-threatening or additive to either withdrawal scenario.

additive to either withdrawal scenario. Uh but again if it it is on its own

Uh but again if it it is on its own independent opioid withdrawal is not

independent opioid withdrawal is not necessarily life-threatening.

necessarily life-threatening. So, uh, kind of jumping back into some

So, uh, kind of jumping back into some toxicities again. Now that we talked a

toxicities again. Now that we talked a little bit about withdrawals, uh,

little bit about withdrawals, uh, talking about alcohol toxicity, not

talking about alcohol toxicity, not necessarily specifically related to

necessarily specifically related to ethanol, but some of the toxic alcohols,

ethanol, but some of the toxic alcohols, namely here like ethylene glycol or

namely here like ethylene glycol or methanol, which can be metabolized to

methanol, which can be metabolized to these very toxic subcomponents. So with

these very toxic subcomponents. So with ethylene glycol you can metabolize it

ethylene glycol you can metabolize it through the normal oxidative p or normal

through the normal oxidative p or normal metabolic pathway of alcohol then

metabolic pathway of alcohol then aldahhide dehydrogenase to a toxic

aldahhide dehydrogenase to a toxic metabolite called oxaloacetate or

metabolite called oxaloacetate or glycolytic acid. You can also produce

glycolytic acid. You can also produce which form these uh crystals and stones

which form these uh crystals and stones in your plasma which migrate down in

in your plasma which migrate down in various capacities to different tissues

various capacities to different tissues but in your kidneys can actually produce

but in your kidneys can actually produce quite rapid uh uh uh kidney toxicity

quite rapid uh uh uh kidney toxicity that uh that can prevent and ultimately

that uh that can prevent and ultimately lead to lead to uh renal failure. uh in

lead to lead to uh renal failure. uh in hypothetically uh chronic issues or

hypothetically uh chronic issues or hypothetically death in that scenario.

hypothetically death in that scenario. Now methanol on the other hand is

Now methanol on the other hand is metabolized to uh uh formaldahhide and

metabolized to uh uh formaldahhide and formic acid which can cause uh uh these

formic acid which can cause uh uh these uh optic nerve issues and optic nerve

uh optic nerve issues and optic nerve demation uh which can c lead to optic

demation uh which can c lead to optic nuritis or even blindness in nu numerous

nuritis or even blindness in nu numerous capacities. So in order to try to

capacities. So in order to try to prevent these toxicities from occurring

prevent these toxicities from occurring uh all we have to do is shut down the

uh all we have to do is shut down the metabolism of these uh alcohols by

metabolism of these uh alcohols by abrupting that pathway. So the one of

abrupting that pathway. So the one of the simplest ways of doing that is

the simplest ways of doing that is actually administering ethanol which has

actually administering ethanol which has a higher affinity for alcohol and

a higher affinity for alcohol and aldahhide dehydrogenase where you're

aldahhide dehydrogenase where you're busy metabolizing this and deferring the

busy metabolizing this and deferring the ethylene glycol and methanol to more

ethylene glycol and methanol to more oxidative pathways which can eliminate

oxidative pathways which can eliminate it or if the patient meets criteria for

it or if the patient meets criteria for hemodilysis you can actually pull it out

hemodilysis you can actually pull it out in that manner too. Um but another agent

in that manner too. Um but another agent we can use is uh frazzole which actually

we can use is uh frazzole which actually acts on the um on a different pathway

acts on the um on a different pathway where we can actually prevent some of

where we can actually prevent some of the metabolites not specifically alcohol

the metabolites not specifically alcohol and alahhide dehydrogenase but we can

and alahhide dehydrogenase but we can prevent the alcohol dehydrogenase from

prevent the alcohol dehydrogenase from occurring uh and metabolizing these

occurring uh and metabolizing these pathways and we can administer it

pathways and we can administer it introvenously. Whereas alcohol we

introvenously. Whereas alcohol we reserve it typically orally uh in some

reserve it typically orally uh in some capacities but you can also

capacities but you can also hypothetically give it introvenously but

hypothetically give it introvenously but most patients can't tolerate it for

most patients can't tolerate it for numerous capacities but for famephasol

numerous capacities but for famephasol um is something that we can give

um is something that we can give parentally uh and for these patients.

parentally uh and for these patients. Another key factor here with famezol is

Another key factor here with famezol is that although again we don't focus on

that although again we don't focus on dosing for many many things here the

dosing for many many things here the dosing for this capacity is actually

dosing for this capacity is actually quite relevant s since it is one of the

quite relevant s since it is one of the few auto-inducers that we know in drug

few auto-inducers that we know in drug therapy. So what another auto-inducer

therapy. So what another auto-inducer would be carbomasopene and if you can

would be carbomasopene and if you can remember back to carbomasopene initial

remember back to carbomasopene initial dosing you have one initial loading dose

dosing you have one initial loading dose you titrate it to a secondary uh loading

you titrate it to a secondary uh loading dose and then you have a tertiary kind

dose and then you have a tertiary kind of chronic maintenance dose and with

of chronic maintenance dose and with fmezol you have a similar scenario where

fmezol you have a similar scenario where we start with 50 milligram per kilogram

we start with 50 milligram per kilogram as a loading dose. Then you give four

as a loading dose. Then you give four doses of 10 milligram per kilogram for a

doses of 10 milligram per kilogram for a 12-h hour increments but then you go

12-h hour increments but then you go back up to 50 milligram per kilogram

back up to 50 milligram per kilogram every 12 hours because we've induced its

every 12 hours because we've induced its autoinduction hypatically. Now there's

autoinduction hypatically. Now there's other supportive care measures you do

other supportive care measures you do want to make sure that we're giving in

want to make sure that we're giving in these scenarios namely um sodium

these scenarios namely um sodium bicarbonate but also a lot of other uh B

bicarbonate but also a lot of other uh B vitamins. So uh puroxine and thymine as

vitamins. So uh puroxine and thymine as well as folic acid which are going to

well as folic acid which are going to help uh if there are any of these toxin

help uh if there are any of these toxin metabolites we are going to be able to

metabolites we are going to be able to intervene by adding these uh uh vitamin

intervene by adding these uh uh vitamin agents to try to uh de detoxify them or

agents to try to uh de detoxify them or metabolize them into more water-soluble

metabolize them into more water-soluble more non-toxic uh metabolites that we

more non-toxic uh metabolites that we can eliminate either hypatically or

can eliminate either hypatically or reiny.

reiny. So inetamine toxicity again we were kind

So inetamine toxicity again we were kind of alluding to this in the past with uh

of alluding to this in the past with uh some of the agents that are stimulating

some of the agents that are stimulating some of these neurologic pathways

some of these neurologic pathways largely related to uh sympathetic neuro

largely related to uh sympathetic neuro neurotransmission but you can also

neurotransmission but you can also activate quite a lot of other neurologic

activate quite a lot of other neurologic pathways including uh dopamine as well

pathways including uh dopamine as well as serotonin uh uh neurologic pathways

as serotonin uh uh neurologic pathways by abusing some of these agents and

by abusing some of these agents and oftentimes we kind of see these

oftentimes we kind of see these clinically used in many pediatric

clinically used in many pediatric patients with uh ADHD or other learning

patients with uh ADHD or other learning deficits that are on a chronic

deficits that are on a chronic empetamine uh uh therapy uh but they can

empetamine uh uh therapy uh but they can evolve into either abuse of those agents

evolve into either abuse of those agents in numerous different capacities or

in numerous different capacities or utilizing these impetamines as uh

utilizing these impetamines as uh outpatient you know uh abuse agents in

outpatient you know uh abuse agents in general. So we can send them to

general. So we can send them to methamphetamines also or other agents

methamphetamines also or other agents like bath salts which we've equated into

like bath salts which we've equated into numerous different capacities that are

numerous different capacities that are analoges of the methyloneetamine pathway

analoges of the methyloneetamine pathway uh that can also stimulate this

uh that can also stimulate this neurologic pathway in numerous different

neurologic pathway in numerous different capacities. But otherwise in the abuse

capacities. But otherwise in the abuse setting in these scenarios or an

setting in these scenarios or an overdose setting the patients are going

overdose setting the patients are going to be very stimulated very uh centrally

to be very stimulated very uh centrally actively stimulated to the point where

actively stimulated to the point where you're seeing a lot of these uh normal

you're seeing a lot of these uh normal agitation symptoms but almost excessive

agitation symptoms but almost excessive where they're getting anxiety

where they're getting anxiety diapharesis hypothermia they could even

diapharesis hypothermia they could even hallucinate even progress to seizures.

hallucinate even progress to seizures. Now the diagnosis and identifying

Now the diagnosis and identifying whether these patients have been abusing

whether these patients have been abusing these is somewhat complex. So we can get

these is somewhat complex. So we can get as best history as we can. But

as best history as we can. But ultimately here again the drug therapy

ultimately here again the drug therapy we're doing in these clinical scenarios

we're doing in these clinical scenarios is trying to treat the symptoms uh while

is trying to treat the symptoms uh while identifying the drug therapy. But again,

identifying the drug therapy. But again, it's largely benzoizopene therapy.

it's largely benzoizopene therapy. Either using something with an active

Either using something with an active metabolite like benzod daipopam or

metabolite like benzod daipopam or mazzlam to try to prolong our

mazzlam to try to prolong our therapeutic effect, but also managing

therapeutic effect, but also managing some of the secondary effects like the

some of the secondary effects like the hypothermia

hypothermia and muscle rigidity that could be

and muscle rigidity that could be accompanying uh these inetamines by just

accompanying uh these inetamines by just providing these cooling parameters like

providing these cooling parameters like cooling blankets or uh introvenous

cooling blankets or uh introvenous cooling liquid like just cooled normal

cooling liquid like just cooled normal saline. Now somewhat related to the in

saline. Now somewhat related to the in amphetamine although somewhat distant to

amphetamine although somewhat distant to it also physiologically is cocaine. Now

it also physiologically is cocaine. Now cocaine abuse uh can be uh thought of as

cocaine abuse uh can be uh thought of as you know the white powder that you've

you know the white powder that you've seen in movies or in different

seen in movies or in different environments where patients have sorted

environments where patients have sorted uh or it could be extended to a a

uh or it could be extended to a a crystal formulation of it uh which is

crystal formulation of it uh which is abused in in in numerous capacities but

abused in in in numerous capacities but smoked uh and sometimes also still

smoked uh and sometimes also still ingested or uh injected in and of

ingested or uh injected in and of itself. But with cocaine oftent times we

itself. But with cocaine oftent times we see a lot of extensive and excessive

see a lot of extensive and excessive central and peripheral inhibition of uh

central and peripheral inhibition of uh uh monoamine reuptake which leads to a

uh monoamine reuptake which leads to a lot of secondary effects like sodium

lot of secondary effects like sodium channel blockade and cardiac

channel blockade and cardiac neurological uh misconductions. So

neurological uh misconductions. So oftentimes we see a lot of these

oftentimes we see a lot of these patients which have abused cocaine

patients which have abused cocaine presented to the emergency department

presented to the emergency department with a lot of chest pain or neurologic

with a lot of chest pain or neurologic issues which could be deemed as kind of

issues which could be deemed as kind of lumped into an acute uh MI scenario. But

lumped into an acute uh MI scenario. But our our treatment necessarily

our our treatment necessarily differentiate once we've identified if

differentiate once we've identified if it is definitively cocaine on board

it is definitively cocaine on board where we're not necessarily giving uh a

where we're not necessarily giving uh a lot of uh uh you know blood thinners or

lot of uh uh you know blood thinners or salicellates in this setting but we're

salicellates in this setting but we're just trying to treat the cocaine which

just trying to treat the cocaine which is largely related to uh kind of

is largely related to uh kind of counteracting the central and peripheral

counteracting the central and peripheral neurological effects by giving

neurological effects by giving bzzoipines again. So again, we're not

bzzoipines again. So again, we're not trying to reinvent the wheel with

trying to reinvent the wheel with bzzoipines since it can be used a lot in

bzzoipines since it can be used a lot in these scenarios, but again, we're trying

these scenarios, but again, we're trying to address this situation. If we can

to address this situation. If we can address it by giving a bzzoizopipene,

address it by giving a bzzoizopipene, we're going to do that as best as

we're going to do that as best as possible by giving it to these patients

possible by giving it to these patients with cocaine abuse. Now, one caveat here

with cocaine abuse. Now, one caveat here that I didn't list is again if a patient

that I didn't list is again if a patient presents with cocaine toxicity uh and it

presents with cocaine toxicity uh and it has an acute mioardial uh issue going

has an acute mioardial uh issue going on, the controversy here is whether or

on, the controversy here is whether or not they can get a beta blocker uh in in

not they can get a beta blocker uh in in that setting. So mettopriol would be

that setting. So mettopriol would be something that would come up related to

something that would come up related to an acute MI management. Now because we

an acute MI management. Now because we know if we block the beta 1 and

know if we block the beta 1 and hypothetically beta 2 receptor uh in

hypothetically beta 2 receptor uh in this setting uh with cocaine with this

this setting uh with cocaine with this sympathetic activation we're going to

sympathetic activation we're going to have an unopposed activation of uh the

have an unopposed activation of uh the alpha or alpha receptors which were

alpha or alpha receptors which were further exacerbate vis constriction and

further exacerbate vis constriction and oxygenation to the tissues. So you can

oxygenation to the tissues. So you can actually exacerbate the cocaine induced

actually exacerbate the cocaine induced chest pain definitively leading to

chest pain definitively leading to myioardial eskemia if you get a beta

myioardial eskemia if you get a beta blocker in this scenario. So that would

blocker in this scenario. So that would be something hypothetically that could

be something hypothetically that could come up on a board exam.

come up on a board exam. Now uh alluding to and jumping into some

Now uh alluding to and jumping into some hallucinogens. Now the hallucinogen is a

hallucinogens. Now the hallucinogen is a a very very broad uh spectrum of agents

a very very broad uh spectrum of agents that patients and and people are going

that patients and and people are going to take as an outpatient setting to try

to take as an outpatient setting to try to essentially create these uh visions

to essentially create these uh visions and issues that they might try to

and issues that they might try to resolve. And and you might see a lot of

resolve. And and you might see a lot of times in different resources uh

times in different resources uh mushrooms are involved in this although

mushrooms are involved in this although I'm going to touch on mushrooms in a

I'm going to touch on mushrooms in a little bit but also some other agents

little bit but also some other agents like DMT uh which can induce a lot of

like DMT uh which can induce a lot of this hallucination activity but is quite

this hallucination activity but is quite short acting uh but you can extend it to

short acting uh but you can extend it to something like LSD uh which is causing

something like LSD uh which is causing quite a prolonged duration of

quite a prolonged duration of hallucinations even to something like uh

hallucinations even to something like uh um more prolonged agents like a

um more prolonged agents like a derivative of ketamine uh that has been

derivative of ketamine uh that has been used uh uh quite extensively in in the

used uh uh quite extensively in in the in the culture. which can lead to a lot

in the culture. which can lead to a lot of hallucinations and delirium uh that

of hallucinations and delirium uh that can lead to uh clinical presentation.

can lead to uh clinical presentation. But again, these patients can present

But again, these patients can present with altermental status coming to the

with altermental status coming to the emergency department or different care

emergency department or different care settings and and and likely have an

settings and and and likely have an exacerbation of these hallucinations

exacerbation of these hallucinations relating to the agitation and and and

relating to the agitation and and and and anxiety and anxiety that's being

and anxiety and anxiety that's being produced. Now we can go through a lot of

produced. Now we can go through a lot of different pathways that we can further

different pathways that we can further delineate and diagnose these patients.

delineate and diagnose these patients. But again coming back to the basic

But again coming back to the basic treatment we're trying to treat them

treatment we're trying to treat them symptomatically if they have hypothermia

symptomatically if they have hypothermia underlying or rigidity treat with that

underlying or rigidity treat with that but also underlying uh treatment here is

but also underlying uh treatment here is largely just benzoizipines and trying to

largely just benzoizipines and trying to aggressively manage them. Now when I was

aggressively manage them. Now when I was talking about inetamines I was kind of

talking about inetamines I was kind of alluding to some other agents that are

alluding to some other agents that are sometimes looped into it but

sometimes looped into it but structurally and somewhat

structurally and somewhat physiologically act differently and

physiologically act differently and those are um the methylinetamines. But

those are um the methylinetamines. But here again not getting into that in too

here again not getting into that in too depth. Meth the methyl xanthines are

depth. Meth the methyl xanthines are somewhat different in the capacity that

somewhat different in the capacity that uh we can abuse them in different

uh we can abuse them in different capacities without even knowing about

capacities without even knowing about it. So methylanthine that does come up

it. So methylanthine that does come up uh quite often is co is caffeine or

uh quite often is co is caffeine or theopheline or theob broine which is

theopheline or theob broine which is found in chocolates. Uh but there they

found in chocolates. Uh but there they have been abused in numerous different

have been abused in numerous different capacities in exercise or or uh if

capacities in exercise or or uh if patients are trying to avoid falling

patients are trying to avoid falling asleep by ingesting a lot of caffeine.

asleep by ingesting a lot of caffeine. they can kind of get to this point where

they can kind of get to this point where they're uh experiencing an excessive

they're uh experiencing an excessive release of endogenous catakolamines and

release of endogenous catakolamines and uh experiencing all this inden uh uh

uh experiencing all this inden uh uh adenazine antagonism uh ultimately

adenazine antagonism uh ultimately leading to quite a lot of uh

leading to quite a lot of uh catakolamine concentration changes and

catakolamine concentration changes and all a whole range of active uh

all a whole range of active uh physiologic effects leading from

physiologic effects leading from agitation cardiac arhythmias CNF CNS

agitation cardiac arhythmias CNF CNS differentiation and ultramental status

differentiation and ultramental status leading to tremors and seizures uh which

leading to tremors and seizures uh which is definitively life-threatening.

is definitively life-threatening. Now, if we can intervene on these

Now, if we can intervene on these patients quite early on, uh we can give

patients quite early on, uh we can give them activated charcoal. And this is one

them activated charcoal. And this is one of the scenarios where we might actually

of the scenarios where we might actually give multiple doses of activated

give multiple doses of activated charcoal at every four to six hour uh

charcoal at every four to six hour uh interval where we're actually going to

interval where we're actually going to try to create a lumin in the gut where

try to create a lumin in the gut where we're going to uh based on interopatic

we're going to uh based on interopatic recirculation pull in from the

recirculation pull in from the circulation these methylanthines back

circulation these methylanthines back into the gut and secure them in the in

into the gut and secure them in the in the charcoal. Try to help eliminate them

the charcoal. Try to help eliminate them as much as possible. But otherwise if we

as much as possible. But otherwise if we can't really uh do anything else in

can't really uh do anything else in these patients again it really comes

these patients again it really comes back to treating their symptomatic uh

back to treating their symptomatic uh seizure and alternal status with

seizure and alternal status with bzzodiaines. Now again kind of jumping

bzzodiaines. Now again kind of jumping on a caffeine just as a key example. One

on a caffeine just as a key example. One of the key uh toxic doses for that is

of the key uh toxic doses for that is about 100 to 150 milligram per kilogram.

about 100 to 150 milligram per kilogram. And the easiest way to remember that is

And the easiest way to remember that is it's about a a cup of coffee per uh uh

it's about a a cup of coffee per uh uh gram or per kilogram of body weight is a

gram or per kilogram of body weight is a lethal dose. So every cup of coffee or

lethal dose. So every cup of coffee or coffee you have has about 100 to 150

coffee you have has about 100 to 150 milligrams of caffeine in it. So you'd

milligrams of caffeine in it. So you'd have to drink uh you know if you weigh

have to drink uh you know if you weigh 80 kilograms 80 cups of coffee uh to be

80 kilograms 80 cups of coffee uh to be able to get a hypothetically

able to get a hypothetically life-threatening dose. Now I will say in

life-threatening dose. Now I will say in numerous different capacities in case in

numerous different capacities in case in case reports we've seen patients die at

case reports we've seen patients die at very lower doses because they have other

very lower doses because they have other underlying cardiac uh issues or cardiac

underlying cardiac uh issues or cardiac eskemia going otherwise that can

eskemia going otherwise that can exacerbate it with a caffeine. But it's

exacerbate it with a caffeine. But it's something to keep in mind that the dose

something to keep in mind that the dose is actually quite high in a in a in a

is actually quite high in a in a in a coffee consumption. But if you looked at

coffee consumption. But if you looked at energy drinks or uh oral caffeine

energy drinks or uh oral caffeine products it's actually quite a lot uh

products it's actually quite a lot uh quite high doses in in very small dosage

quite high doses in in very small dosage form. So an over-the-c counter caffeine

form. So an over-the-c counter caffeine product uh you can buy is 200 milligrams

product uh you can buy is 200 milligrams of caffeine per tablet. So if you go to

of caffeine per tablet. So if you go to Sam's Club or Costco, you can buy 500

Sam's Club or Costco, you can buy 500 tablets and if you ingest a hundred of

tablets and if you ingest a hundred of them, that's a potentially fatal dose

them, that's a potentially fatal dose and they're actually quite small. So you

and they're actually quite small. So you ingest them quite a lot quite rapidly.

ingest them quite a lot quite rapidly. Um which is very concerning for the

Um which is very concerning for the patient. So multiple dose activated

patient. So multiple dose activated charcoal would definitely hone in on on

charcoal would definitely hone in on on those patient scenarios. Now, I was

those patient scenarios. Now, I was alluding to mushrooms in the

alluding to mushrooms in the hallucinogen section, but mushrooms is

hallucinogen section, but mushrooms is quite a large large uh class of plants

quite a large large uh class of plants uh that patients can ingest. And there's

uh that patients can ingest. And there's uh ultimately 14 different subcategories

uh ultimately 14 different subcategories of toxic mushrooms. And I won't go into

of toxic mushrooms. And I won't go into any of them in any depth, but the the

any of them in any depth, but the the treatment here is related explicitly to

treatment here is related explicitly to the type of mushroom that was ingested.

the type of mushroom that was ingested. So, say it was something like an

So, say it was something like an ammonita

ammonita or ammonita uh species mushroom that the

or ammonita uh species mushroom that the patient has ingested. Now that is again

patient has ingested. Now that is again you don't necessarily need to remember

you don't necessarily need to remember the name but that almost is always

the name but that almost is always entirely related to physiology

entirely related to physiology physiology related to acetaminophen

physiology related to acetaminophen toxicity where you have this

toxicity where you have this intereroatic

intereroatic toxicity and we treat it almost

toxicity and we treat it almost similarly with an acetylcysteine and you

similarly with an acetylcysteine and you can also extrapolate it to acabin to

can also extrapolate it to acabin to treat that uh patient with that toxicity

treat that uh patient with that toxicity but we'd equate it also to uh uh

but we'd equate it also to uh uh different mushrooms that patients are

different mushrooms that patients are ingesting nowadays which is gaining

ingesting nowadays which is gaining quite a lot of popularity and neurotypic

quite a lot of popularity and neurotypic capacity ities um like psilocybin

capacity ities um like psilocybin uh mushrooms that are more hallucinogens

uh mushrooms that are more hallucinogens uh that aren't necessarily

uh that aren't necessarily life-threatening if they're ingested on

life-threatening if they're ingested on their own but can lead to other

their own but can lead to other life-threatening scenarios. So if we can

life-threatening scenarios. So if we can treat that patient necessarily in a

treat that patient necessarily in a withdrawal setting it's largely just a

withdrawal setting it's largely just a bzzoipene. So with mushroom toxicity, if

bzzoipene. So with mushroom toxicity, if you can identify the type of mushroom

you can identify the type of mushroom that has been ingested, uh identify the

that has been ingested, uh identify the onset of symptoms and the timeline for

onset of symptoms and the timeline for that, you can try to differentiate and

that, you can try to differentiate and narrow down which type of mushroom

narrow down which type of mushroom they've actually ingested to try to

they've actually ingested to try to identify which treatment pathway they

identify which treatment pathway they actually definitively need to be on. But

actually definitively need to be on. But almost always in these scenarios, I'd

almost always in these scenarios, I'd recommend consulting the poison center

recommend consulting the poison center to try try to get a toxicologist on

to try try to get a toxicologist on board to try to help you through um

board to try to help you through um identifying which mushroom specy it was.

identifying which mushroom specy it was. And also one key point in clinical pearl

And also one key point in clinical pearl here, if you have a patient in the acute

here, if you have a patient in the acute care setting that has brought in the

care setting that has brought in the mushrooms that they ingested

mushrooms that they ingested accidentally, if you can put them in a

accidentally, if you can put them in a paper bag as soon as possible rather

paper bag as soon as possible rather than a plastic bag, you can actually uh

than a plastic bag, you can actually uh preserve the function and the structure

preserve the function and the structure of those mushrooms and also collect any

of those mushrooms and also collect any of the mushroom spores that

of the mushroom spores that differentiate and drop from the mushroom

differentiate and drop from the mushroom itself to try to have identify that on a

itself to try to have identify that on a lab scale. The poison center might

lab scale. The poison center might actually really enjoy that uh if you

actually really enjoy that uh if you could help them in that capacity. Uh so

could help them in that capacity. Uh so going on to nicotine. So nicotine in

going on to nicotine. So nicotine in itself often we think of uh being

itself often we think of uh being related to uh cigarette consumption or

related to uh cigarette consumption or smoking consumption. Now the toxicity

smoking consumption. Now the toxicity can be related to nicotine uh from that

can be related to nicotine uh from that smoking consumption. But oftentimes we

smoking consumption. But oftentimes we actually see it as an ingested toxic

actually see it as an ingested toxic agent either from the transdermal uh

agent either from the transdermal uh exposure or the oral exposure uh for

exposure or the oral exposure uh for patients that are on uh trying to you

patients that are on uh trying to you know abstain from smoking by using a

know abstain from smoking by using a patch or oral drug therapy with

patch or oral drug therapy with nicotine. But in certain capacities they

nicotine. But in certain capacities they could either abuse it or someone can

could either abuse it or someone can sometimes uh intentionally ingest it in

sometimes uh intentionally ingest it in a potential toxic environment. So what

a potential toxic environment. So what we can see here is somewhat analogous to

we can see here is somewhat analogous to uh the uh acetylcholine receptor uh

uh the uh acetylcholine receptor uh physiology we were talking about with um

physiology we were talking about with um kind of like a anticolinergic colonergic

kind of like a anticolinergic colonergic toxidrome that we were alluding to

toxidrome that we were alluding to earlier on. But there are some key

earlier on. But there are some key differences here with nicotine. But

differences here with nicotine. But again, uh the key points here is to

again, uh the key points here is to remember if they have an early onset,

remember if they have an early onset, it's going to be quite analogous to uh

it's going to be quite analogous to uh uh something related to um uh uh the the

uh something related to um uh uh the the rapid ingestion of it either as a

rapid ingestion of it either as a transdermal or what you can identify,

transdermal or what you can identify, but also just trying to identify what

but also just trying to identify what you can uh potentially reverse in in an

you can uh potentially reverse in in an acute care setting. So if you can

acute care setting. So if you can reserve and remove a patch or administer

reserve and remove a patch or administer charcoal, it's something we can do uh

charcoal, it's something we can do uh through decontamination, but also def

through decontamination, but also def definitively looking at bzzoipines as a

definitively looking at bzzoipines as a supportive care measure. And just to

supportive care measure. And just to kind of wrap up, the last uh one we'll

kind of wrap up, the last uh one we'll really go over here today is

really go over here today is non-benzoizabene sedative toxicity. And

non-benzoizabene sedative toxicity. And it's really analogous to what I was

it's really analogous to what I was alluding to with the sedative hypnotic

alluding to with the sedative hypnotic toxicity where uh we kind of looped in a

toxicity where uh we kind of looped in a number of these different uh toxidromes

number of these different uh toxidromes that kind of share a lot of the GABA

that kind of share a lot of the GABA pathway uh uh stimulation where uh we

pathway uh uh stimulation where uh we really want to intervene as rapidly as

really want to intervene as rapidly as possible. And the key here is if we can

possible. And the key here is if we can identify a patient that maybe has taken

identify a patient that maybe has taken too much of their sleeping aid to really

too much of their sleeping aid to really try to uh help them out by administering

try to uh help them out by administering quite a lot of benzoazipene um and and

quite a lot of benzoazipene um and and and support them supportively. But in

and support them supportively. But in some capacities, uh, if they've

some capacities, uh, if they've excessively ingested this, a fluanol

excessively ingested this, a fluanol could be an option that we would

could be an option that we would consider. Now, I know we're kind of

consider. Now, I know we're kind of running short on time, but I did want

running short on time, but I did want to, uh, turn it over for some any

to, uh, turn it over for some any questions that we could try to help

questions that we could try to help answer if we have any time left. Uh, but

answer if we have any time left. Uh, but if if there is anything else we could

if if there is anything else we could try to intervene on in that capacity, we

try to intervene on in that capacity, we could definitely try to do so, uh, in in

could definitely try to do so, uh, in in the time the time frame we've got left

the time the time frame we've got left here.

here. >> Yeah. Yeah, I mean I think there's a

>> Yeah. Yeah, I mean I think there's a question about um can we compare NMS? I

question about um can we compare NMS? I mean, we've kind of alluded to this

mean, we've kind of alluded to this already, but can we compare compare NMS

already, but can we compare compare NMS hypothermia and the potential need for

hypothermia and the potential need for dantelene in the ER?

dantelene in the ER? I've never used Dantrine in the

I've never used Dantrine in the emergency department and never have

emergency department and never have needed it. Um because quite honestly the

needed it. Um because quite honestly the h malignant hypothermia that occurs is

h malignant hypothermia that occurs is almost always in the context of a um o

almost always in the context of a um o scenario.

scenario. >> Yeah, I would fully agree with that. Um

>> Yeah, I would fully agree with that. Um and oftentimes if it is alluding to a

and oftentimes if it is alluding to a dantine scenario, we just haven't dosed

dantine scenario, we just haven't dosed the benzoizopene appropriately to that

the benzoizopene appropriately to that to that patient. Um so we just need to

to that patient. Um so we just need to optimize that drug therapy. uh second

optimize that drug therapy. uh second line we'd add on something like uh a

line we'd add on something like uh a pheninoarbatital even third line the

pheninoarbatital even third line the patient's going to get uh you know

patient's going to get uh you know propall or something extensive from that

propall or something extensive from that and then hypothetically we haven't even

and then hypothetically we haven't even addressed what's going on maybe

addressed what's going on maybe hypothetically you could consider

hypothetically you could consider dancing but I mean it's really really

dancing but I mean it's really really it's definitely not something I' I've

it's definitely not something I' I've actually even ever used myself. Yeah, I

actually even ever used myself. Yeah, I mean just think of Dantrilene as really

mean just think of Dantrilene as really to target the rhyodine receptor for

to target the rhyodine receptor for patients who have a genetic

patients who have a genetic predisposition for this and it's it's

predisposition for this and it's it's very rare and typically only occurs in

very rare and typically only occurs in the context of the O whereas neurolptic

the context of the O whereas neurolptic malignant syndrome has manifestations

malignant syndrome has manifestations clinically that look very similar muscle

clinically that look very similar muscle rigidity altered mental status

rigidity altered mental status hypothermia sweating they're you know

hypothermia sweating they're you know tacocartic

tacocartic um and you're going to still use

um and you're going to still use benzoazipines you want to relax them you

benzoazipines you want to relax them you want to calm their sympathetic tone um

want to calm their sympathetic tone um so that you the muscle breakdown isn't

so that you the muscle breakdown isn't happening and then you give

happening and then you give anticolinergic drugs to basically kind

anticolinergic drugs to basically kind of create balance. So if you think of

of create balance. So if you think of the extreme version of Parkinson's

the extreme version of Parkinson's disease essentially what you're trying

disease essentially what you're trying to do is break that imbalance by giving

to do is break that imbalance by giving anticolinergic drugs and then loosening

anticolinergic drugs and then loosening their muscles. Um the next question came

their muscles. Um the next question came up of I'm I can't convince my hospital

up of I'm I can't convince my hospital to carry adex alpha for factor 10A meds.

to carry adex alpha for factor 10A meds. They are all about Kentra. Does your

They are all about Kentra. Does your hospital system carry both? Have you

hospital system carry both? Have you found Nexon Dex alpha to be far

found Nexon Dex alpha to be far superior?

superior? Uh I don't carry both at my hospital. We

Uh I don't carry both at my hospital. We still use uh Kentra uh for almost any

still use uh Kentra uh for almost any type of bleed except for Digitran where

type of bleed except for Digitran where we have index or um prabine.

we have index or um prabine. uh the evidence is somewhat limited in a

uh the evidence is somewhat limited in a comparison setting since it's really

comparison setting since it's really never been definitively compared in a

never been definitively compared in a good clinical setting in a clinical

good clinical setting in a clinical trial. It's almost like a single arm

trial. It's almost like a single arm trial that we've seen in either agent.

trial that we've seen in either agent. So there's no good competitive

So there's no good competitive >> literature. But in in certain scenarios

>> literature. But in in certain scenarios just discussing with surgeons that have

just discussing with surgeons that have taken these patients to the O uh what

taken these patients to the O uh what I've encountered with at least Kentra is

I've encountered with at least Kentra is that even with if they're on a Pixaban

that even with if they're on a Pixaban or riverox outpatient and we can give

or riverox outpatient and we can give them Kentra in the acute care setting in

them Kentra in the acute care setting in the O they actually have a better

the O they actually have a better control of the the bleeding going on and

control of the the bleeding going on and somewhat administer a little bit less

somewhat administer a little bit less blood product but in that setting it

blood product but in that setting it actually is quite difficult to pull out

actually is quite difficult to pull out the definitive clinical endpoint they

the definitive clinical endpoint they actually need to study other than

actually need to study other than mortality um and it's it's a high

mortality um and it's it's a high mortality scenario anyway

mortality scenario anyway >> and I don't recall the

>> and I don't recall the actual price but you know both of those

actual price but you know both of those antidotes are pretty expensive and I

antidotes are pretty expensive and I mean not that Kencha is cheap

mean not that Kencha is cheap significantly cheap or you know like

significantly cheap or you know like nothing but it's still a lot less and so

nothing but it's still a lot less and so when you

when you >> you don't really have a clear efficacy

>> you don't really have a clear efficacy point you got a cost association with it

point you got a cost association with it and quite honestly it's

and quite honestly it's I'm not saying

I'm not saying impossible but it's pretty rare that

impossible but it's pretty rare that people come in with that scenario that

people come in with that scenario that we have to reverse them that acutely

we have to reverse them that acutely um and but the one thing I will say

um and but the one thing I will say about Kentra is you know you can go the

about Kentra is you know you can go the other extreme too um then there's a

other extreme too um then there's a reason the patient needs to be on

reason the patient needs to be on antiquagulant you can overly um provide

antiquagulant you can overly um provide them too much and create a

them too much and create a pro-thrombotic or a thrombotic in uh

pro-thrombotic or a thrombotic in uh environment so uh I've I my emergency

environment so uh I've I my emergency department group we do work with

department group we do work with multiple institutions in a larger

multiple institutions in a larger geographic region and all of those

geographic region and all of those hospitals um only have K centra.

hospitals um only have K centra. So the next question is uh would you

So the next question is uh would you give digifab

give digifab in hypercalemia and this was in the I

in hypercalemia and this was in the I think at the time uh Jennifer asked this

think at the time uh Jennifer asked this question in in the context of deoxin

question in in the context of deoxin overdose. So you have ded deoxxin

overdose. So you have ded deoxxin overdose you get hypercalemic. So now

overdose you get hypercalemic. So now everybody wants to treat the

everybody wants to treat the hypercalemia as hypercalemia

hypercalemia as hypercalemia >> and what you know versus understanding

>> and what you know versus understanding what is happening with the potassium in

what is happening with the potassium in the context of dig overdose. So one

the context of dig overdose. So one thing that's important for you guys to

thing that's important for you guys to remember is the the uh potassium level

remember is the the uh potassium level at the time of the dig overdose is

at the time of the dig overdose is prognostic. If it if it's elevated and

prognostic. If it if it's elevated and they're hypercalemic they they almost

they're hypercalemic they they almost never make it. Um so you got to be

never make it. Um so you got to be really careful you know in that

really careful you know in that situation. why we check for it. But if

situation. why we check for it. But if you think about the mechanism, it's a

you think about the mechanism, it's a sodium potassium ATPAS pump inhibitor.

sodium potassium ATPAS pump inhibitor. So it's basically blocking that

So it's basically blocking that exchange. And where does potassium

exchange. And where does potassium normally reside? Well, it's a major

normally reside? Well, it's a major intracellular cation. So if you're

intracellular cation. So if you're blocking it from being able to go back

blocking it from being able to go back inside the cell, it's sitting outside of

inside the cell, it's sitting outside of the cell. You know, total body potassium

the cell. You know, total body potassium levels aren't changing. It's just where

levels aren't changing. It's just where is the potassium residing? Um I don't

is the potassium residing? Um I don't know Craig do you want to talk about

know Craig do you want to talk about because the question is really about

because the question is really about calcium gluconate um and should we treat

calcium gluconate um and should we treat like traditional hypercalemia and I

like traditional hypercalemia and I think we brought this up in a previous

think we brought this up in a previous session of the theoretical stoned heart

session of the theoretical stoned heart scenario where you know deoxxin

scenario where you know deoxxin increases intracellular calcium

increases intracellular calcium concentrations. So do I give them

concentrations. So do I give them calcium gluconate with EKG changes as

calcium gluconate with EKG changes as I'm getting ready to drive the potassium

I'm getting ready to drive the potassium back in the cell?

back in the cell? Yeah, I mean it is and the evidence is

Yeah, I mean it is and the evidence is somewhat clinically controversial

somewhat clinically controversial because again the past time we were

because again the past time we were talking about it um the recent evidence

talking about it um the recent evidence that had come out from the one of the

that had come out from the one of the poison center looking at a lot of these

poison center looking at a lot of these cases almost 3,000 cases uh of dioxin

cases almost 3,000 cases uh of dioxin toxicity where there was hypercalemia

toxicity where there was hypercalemia they did get digifab but they actually

they did get digifab but they actually got calcium administered in that acute

got calcium administered in that acute care setting and the there was no

care setting and the there was no excessive mortality uh related to that

excessive mortality uh related to that um no stone part been observed

um no stone part been observed clinically. However, again kind of

clinically. However, again kind of relating back you haven't necessarily

relating back you haven't necessarily fully obligated the risk of uh stone

fully obligated the risk of uh stone heart or cardiac you know impairing

heart or cardiac you know impairing cardiac contractility by giving calcium

cardiac contractility by giving calcium uh in that setting. So the the the thing

uh in that setting. So the the the thing that I try to emphasize is that if we

that I try to emphasize is that if we have a a definitive patient with a

have a a definitive patient with a detoxin toxicity going on the definitive

detoxin toxicity going on the definitive treatment is digifab um we can treat

treatment is digifab um we can treat their hypercalemia also that's very

their hypercalemia also that's very important to do and we can treat it very

important to do and we can treat it very aggressively with our normal regimen of

aggressively with our normal regimen of insulin sodium bicarbonate we can give

insulin sodium bicarbonate we can give some uh renal limiting agent if they

some uh renal limiting agent if they have intact renal function like

have intact renal function like ferosomide or bummetide um even

ferosomide or bummetide um even albuterol uh to try to dissipate and

albuterol uh to try to dissipate and redistribute the potassium or the

redistribute the potassium or the potassium but what we don't want to do

potassium but what we don't want to do and we can abstain from gaming calcium

and we can abstain from gaming calcium in that setting because we have all

in that setting because we have all these other agents we could

these other agents we could hypothetically use. So if we can do it

hypothetically use. So if we can do it early on it's somewhat advantageous but

early on it's somewhat advantageous but um hypothetically you could be in a

um hypothetically you could be in a scenario where you don't know they're

scenario where you don't know they're necessarily ditch toxic. You treat their

necessarily ditch toxic. You treat their hypercalemia because that came back

hypercalemia because that came back first and then now you have a lab that

first and then now you have a lab that just came back with a dig level that we

just came back with a dig level that we didn't even know the patient was on and

didn't even know the patient was on and we've been treating their potassium

we've been treating their potassium their calcium had been administered and

their calcium had been administered and you just try to observe the patient for

you just try to observe the patient for any cardiac contractility issues they

any cardiac contractility issues they could hypothetically intervene on. Uh

could hypothetically intervene on. Uh but again it's it's really it's it's

but again it's it's really it's it's it's a clinical controversy that um

it's a clinical controversy that um depending on who you talk to you're

depending on who you talk to you're going to have definitive answers. So on

going to have definitive answers. So on the exam I I try to allude to the say

the exam I I try to allude to the say you would avoid calcium in that scenario

you would avoid calcium in that scenario because there are other definitive

because there are other definitive treatments you can give uh to try to

treatments you can give uh to try to answer that question.

answer that question. >> Yeah. I mean I think the chance it

>> Yeah. I mean I think the chance it showing up on a board exam is low

showing up on a board exam is low because it's too controversial without

because it's too controversial without definitive and those do not make board

definitive and those do not make board qu good board questions.

qu good board questions. um they'll have ditch and toxicity but

um they'll have ditch and toxicity but it'll be from another perspective or a

it'll be from another perspective or a concept that they want you to

concept that they want you to understand. Uh so there was a question

understand. Uh so there was a question about can you go over cocaine and MI

about can you go over cocaine and MI again and can you give ledol

again and can you give ledol um so I mean if we think about all the

um so I mean if we think about all the things that affect the hemodynamics of

things that affect the hemodynamics of the vascule and the tone of the vascule

the vascule and the tone of the vascule you've got beta 2 receptors which when

you've got beta 2 receptors which when they're activated are going to dilate uh

they're activated are going to dilate uh those vessels relax them um you have

those vessels relax them um you have alpha receptors in particular that are

alpha receptors in particular that are playing tuck war and they're going to

playing tuck war and they're going to constrict them when they're stimulated.

constrict them when they're stimulated. So if you theoretically block one of

So if you theoretically block one of them, you get unopposed

them, you get unopposed alpha constriction. So a non selective

alpha constriction. So a non selective beta blocker like Lebalo

beta blocker like Lebalo um has that mixed effect, but it also

um has that mixed effect, but it also has alpha 1 blocking properties. So

has alpha 1 blocking properties. So that's the controversy that sort of

that's the controversy that sort of comes up is can we still give ledol in

comes up is can we still give ledol in this situation and and I would just say

this situation and and I would just say this you you the that you've missed the

this you you the that you've missed the first drug of choice which is a benzo

first drug of choice which is a benzo if you're if you're reaching in the bag

if you're if you're reaching in the bag to grab leol

to grab leol you you've missed the first thing right

you you've missed the first thing right because ledol is not your not your focal

because ledol is not your not your focal point

point >> and if you're really worried about basos

>> and if you're really worried about basos spasm and worsening it you should give

spasm and worsening it you should give something that's going to relax the

something that's going to relax the spasm.

spasm. So, you know, you got you got a whole

So, you know, you got you got a whole plethora of drugs, calcium channel

plethora of drugs, calcium channel blockers, you've got, you know,

blockers, you've got, you know, fentalamine that you could theoretically

fentalamine that you could theoretically give um you know, even clonity at some

give um you know, even clonity at some level to, you know, reduce sympathetic

level to, you know, reduce sympathetic tone uh coming out. So I I just I've

tone uh coming out. So I I just I've never needed to use or see ledol in in a

never needed to use or see ledol in in a clinical environment where cocaine or

clinical environment where cocaine or sympathomimedic is causing chest pain or

sympathomimedic is causing chest pain or vaso spasm. I don't know Dr. Cookio, you

vaso spasm. I don't know Dr. Cookio, you can certainly

can certainly >> Yeah, I mean I I I would just say almost

>> Yeah, I mean I I I would just say almost the exact same things. So I just haven't

the exact same things. So I just haven't seen it. If you have an acute MI patient

seen it. If you have an acute MI patient that has like a legitimate MI uh that

that has like a legitimate MI uh that has ingested cocaine also you have the

has ingested cocaine also you have the you know cathide team down at the

you know cathide team down at the bedside and the cardiologist they're

bedside and the cardiologist they're almost never saying give led all uh it's

almost never saying give led all uh it's so many other drug therapies that

so many other drug therapies that they're getting aspirin plavix or you

they're getting aspirin plavix or you know any other antiplelet agent um

know any other antiplelet agent um >> yeah and if they're young patient

>> yeah and if they're young patient >> it's not a beta blocker

>> it's not a beta blocker >> yeah I mean if you're if you're a young

>> yeah I mean if you're if you're a young patient you're 20 years old and you've

patient you're 20 years old and you've snorted too much cocaine you you you

snorted too much cocaine you you you probably don't have aoscerotic disease,

probably don't have aoscerotic disease, right? So, your problem is a vasospasm

right? So, your problem is a vasospasm in most cases. Now, that doesn't mean

in most cases. Now, that doesn't mean that older middle-aged people with

that older middle-aged people with vascular disease don't smoke or and

vascular disease don't smoke or and snort cocaine. They do all the time.

snort cocaine. They do all the time. Even grandpas, you know, do it. I've

Even grandpas, you know, do it. I've seen that. So, don't stereotype. But,

seen that. So, don't stereotype. But, you know, you do need to consider what

you know, you do need to consider what are some of the underlying precipitants.

are some of the underlying precipitants. And certainly, if they have vascular

And certainly, if they have vascular disease, then you you start thinking

disease, then you you start thinking about the other things too. Aspirin and

about the other things too. Aspirin and plavix like Dr. Kokia was saying, but

plavix like Dr. Kokia was saying, but the other the other thing is if they go

the other the other thing is if they go to the Kath lab and they see that it's a

to the Kath lab and they see that it's a vasospasm, which they'll they'll see

vasospasm, which they'll they'll see very quickly when they inject, they'll

very quickly when they inject, they'll just they'll they'll locally inject a

just they'll they'll locally inject a vaso diilator right there to release the

vaso diilator right there to release the spasm. And you know, so it's a mood

spasm. And you know, so it's a mood point I think um that you know, most

point I think um that you know, most people would not give leol because you

people would not give leol because you have so many other options um at your

have so many other options um at your disposal. Can you elaborate a little bit

disposal. Can you elaborate a little bit more what you were saying about the

more what you were saying about the Siwa? Uh I think that was in the context

Siwa? Uh I think that was in the context of the alcohol uh toxicity you were

of the alcohol uh toxicity you were >> I think it was also related to uh the

>> I think it was also related to uh the ICU setting. So if a patient's admitted

ICU setting. So if a patient's admitted to the critical care setting uh we we

to the critical care setting uh we we sometimes use a SEWA scale in that

sometimes use a SEWA scale in that capacity. Other like RAS scales uh might

capacity. Other like RAS scales uh might be utilized also just to assess their

be utilized also just to assess their sedation level, but see what can still

sedation level, but see what can still be used in a critical set care setting

be used in a critical set care setting uh to track their alcohol withdrawal

uh to track their alcohol withdrawal parameters in terms of whether they're

parameters in terms of whether they're not uh having agitation or delirium in

not uh having agitation or delirium in that setting also. Uh but the diff the

that setting also. Uh but the diff the difference being that it hasn't been

difference being that it hasn't been validated in the sense we can

validated in the sense we can definitively use it to improve patient

definitively use it to improve patient outcome in a in a in a in a research

outcome in a in a in a in a research setting. uh but it is used clinically

setting. uh but it is used clinically because there's really no other tool uh

because there's really no other tool uh to utilize. So again if a patient's in a

to utilize. So again if a patient's in a critical care setting you might have

critical care setting you might have other uh tracking parameters which

other uh tracking parameters which aren't definitive but if they're in a

aren't definitive but if they're in a you know just generally admitted you

you know just generally admitted you know normal acute you know acute care

know normal acute you know acute care setting or a nonICU setting a SIA is

setting or a nonICU setting a SIA is definitively validated. So that would

definitively validated. So that would definitely be the right monitoring

definitely be the right monitoring answer. Yeah, I mean these risk

answer. Yeah, I mean these risk stratification tools are are what

stratification tools are are what there's what they are just tools.

there's what they are just tools. They're not

They're not almost nothing in medicine that we use

almost nothing in medicine that we use as a quote unquote monitoring parameter

as a quote unquote monitoring parameter in isolation by itself is going to be

in isolation by itself is going to be defended. You're treating a a complex

defended. You're treating a a complex interaction of scenarios and patients

interaction of scenarios and patients with probably not even just isolated

with probably not even just isolated alcohol use. Um there's probably also

alcohol use. Um there's probably also something else going on or another

something else going on or another coorbidity that's interacting with it.

coorbidity that's interacting with it. And so you want to treat the patient

And so you want to treat the patient clinically and you should be able to

clinically and you should be able to with treat and identify alcohol

with treat and identify alcohol withdrawal and some of its symptoms uh

withdrawal and some of its symptoms uh clinically by just talking to the

clinically by just talking to the patient looking at their vital signs. Uh

patient looking at their vital signs. Uh there was a question from Betsy about

there was a question from Betsy about what is your opinion on fixed doses of

what is your opinion on fixed doses of Kentra

Kentra versus uh weight-based dosing.

versus uh weight-based dosing. >> Yeah. So like I was mentioning like

>> Yeah. So like I was mentioning like clinically there's quite a lot of

clinically there's quite a lot of different dosing. So the packaging

different dosing. So the packaging insert has weight- based dosing. I mean

insert has weight- based dosing. I mean I use fixed fit fixed dosing uh for

I use fixed fit fixed dosing uh for casera in our acute care setting. Even

casera in our acute care setting. Even the protocols that we have in line uh I

the protocols that we have in line uh I use different doses depending on the

use different doses depending on the patient scenario, the individual patient

patient scenario, the individual patient scenario. Uh so it could range from

scenario. Uh so it could range from anywhere from 500 units to 2,000 units

anywhere from 500 units to 2,000 units depending on what's going on uh in that

depending on what's going on uh in that patient. Um and actually so

patient. Um and actually so interestingly there's a lot of

interestingly there's a lot of literature out there but actually was

literature out there but actually was one of the authors on a a major study

one of the authors on a a major study where we looked at uh differentiating

where we looked at uh differentiating different different fixed doses of

different different fixed doses of different PCC agents including FIBA in

different PCC agents including FIBA in that setting at different I think there

that setting at different I think there was six different sites where actually

was six different sites where actually using a retrospective data uh we saw

using a retrospective data uh we saw really no difference in in clinical

really no difference in in clinical outcome but um what was interesting

outcome but um what was interesting there is again there's fixed doses but

there is again there's fixed doses but it could range in in quite uh quite a

it could range in in quite uh quite a lot of capacity. So that's why I was

lot of capacity. So that's why I was kind of alluding to that it's not going

kind of alluding to that it's not going to be on the exam just because there's

to be on the exam just because there's so much different in clinical practice

so much different in clinical practice and also the literature that we see what

and also the literature that we see what is the right fixed doses. It's hard to

is the right fixed doses. It's hard to hard to discern enough to be on the exam

hard to discern enough to be on the exam itself.

itself. >> Yeah. I mean the boards want to make

>> Yeah. I mean the boards want to make sure that you pick the right scenario or

sure that you pick the right scenario or you know you're you're following a

you know you're you're following a pattern of association that link you to

pattern of association that link you to the right treatment or decision next

the right treatment or decision next level decision. Many times that is not a

level decision. Many times that is not a dose especially when there's ranges that

dose especially when there's ranges that are not definitive. It's not going to be

are not definitive. It's not going to be there. You can't justify it. So

there. You can't justify it. So clinically it's I mean so what we're

clinically it's I mean so what we're having is a clinical discussion here.

having is a clinical discussion here. Knowing that you're going to pick Kentra

Knowing that you're going to pick Kentra in the high risk or life-threatening

in the high risk or life-threatening bleed scenario in the context of some

bleed scenario in the context of some other thing that needs to be reversed is

other thing that needs to be reversed is the answer.

Not not the dose. What else? Those are good questions.

What else? Those are good questions. >> Yeah, good questions.

>> All right. Well, thank you guys. Uh, you know, we've got three minutes left. So,

know, we've got three minutes left. So, um, I know that was a lot of information

um, I know that was a lot of information and, you know, critical care and acute

and, you know, critical care and acute care, emergency medicine. I mean, it's

care, emergency medicine. I mean, it's broad. There's a lot of things to cover,

broad. There's a lot of things to cover, a lot of topics to hit on.

a lot of topics to hit on. uh we try to cover some of the

uh we try to cover some of the non-conventional topics that don't fit

non-conventional topics that don't fit necessarily in a you know organ system

necessarily in a you know organ system as easily and uh to try to make sure we

as easily and uh to try to make sure we hit some of those. So that you've seen

hit some of those. So that you've seen from these series of uh webinars that

from these series of uh webinars that we've been doing where we're hitting on,

we've been doing where we're hitting on, you know, acute care, chronic care

you know, acute care, chronic care scenarios, inpatient, outpatient,

scenarios, inpatient, outpatient, different age groups. Um and that's our

different age groups. Um and that's our goal with the remaining sessions as

goal with the remaining sessions as well. um including even some subsp

well. um including even some subsp specialcialized areas like oncology

specialcialized areas like oncology which we had last time and then again we

which we had last time and then again we tapped into some toxicology because

tapped into some toxicology because those are topics that people tend to

those are topics that people tend to struggle with um more than something

struggle with um more than something like diabetes or dysipidemia which we

like diabetes or dysipidemia which we you know beat to death at nauseium. Um

you know beat to death at nauseium. Um so I'm not saying it's not important or

so I'm not saying it's not important or relevant but the most people are

relevant but the most people are familiar with the core concepts of

familiar with the core concepts of those. So with that we will let you guys

those. So with that we will let you guys go. Thank you and we'll see you again

go. Thank you and we'll see you again soon.

soon. >> Bye.

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YouTube Transcript:Session 4 - Live Rapid Review for BPS Exams