Clinical Judgment and Protocols

[DwayneEMTP]

Happiness made a good point about this possibly being an ex peer...though I can't think of a single one that has such a 3rd grade grasp of grammar....

Also, what is the fixation with me being fired? That seems weird...Nearly every post had something to do with that, and the brilliance of my ex boss for doing so...which brings me back to maybe happiness' post...and my answer again.

There truly isn't anyone that I know that would attack in such a childish way. I have been intellectually pounded by medics/intermediates/and medics alike..but never anyone so ignorant as this.

I'll be curious to see if ak or admin can tie this person to an older ID.

Dwayne

[emtannie]

You idiots on this site have blown me away, this isn't a site for learning. You people are idiots ! Plain and simple. I was on here for a week and am already done. You assholes simply amaze me. You all feed off of each others stupidity. Dwayne , as I said before - you deserved to be fired, why - because you are a strum job... Period...

Wow - I am gone for 24 hours, and I am 5 pages behind on this thread.

Johnboy, twice I have asked you for specific references to show that glucagon intranasally is a superior option. Twice I have asked you to provide your protocol so that we can review it. Twice, you have ignored me.

I see that since I was away, you have posted "references" without actually citing the sources. THis is not just bad form, it will get you a zero grade if you tried this on any paper you tried to hand in in your medic class.

Rather than have intelligent debate, you have resorted to namecalling, rather than citing medical sources to prove your point. Medscape is a good site, but when you can't even attach the link to the information you provide, your post is useless.

So, again, I will ask:

1. Please provide recent medical journal references that specifically refer to glucagon IN as an appropriate intervention, and shows that is has a faster response than glucagon IM.

2. Please provide your local protocol which shows the hypoglycemia algorithm allowing you to use IN glucagon and under what circumstances

3. Can you tell me if you reconstitute the glucagon when you administer it IN, and if you also add a surfactant to it? I am curious.

You have called all of us here "idiots" and stated that "this is not a site for learning." Johnboy, I am trying to learn - I, and others, have researched glucagon IN and haven't been able to find where it is the "current standard" as you have stated, so we are asking you to educate us in this. How can you say that this is not a site for learning? We have asked for the information, you have refused to provide it' therefore, you are the one who is preventing learning, not us.

Johnboy, please note - Dwayne has never stated that he didn't deserve to be fired. In fact, in his first post in this thread, he cautioned Bieber about working outside of protocol, so your continued attacks on him are completely invalid.

Again, until you can provide a post with accurate information, and refrain from name-calling, I will consider you a troll and nothing more.

[island emt]

Dwayne-

Good luck, you are cool on this site , but I am quite sure you are black balled in the real world cowboy!!!

Again- I would have fired you also cowboy!!!

You are not only an idiot, buy a stubborn one at that...

HELLO Kettle this is the POT :-}

My guess is that JB spends far tooo much time on his knees under dwayne's ex bosses desk.

Or it's as annie said a former troll come back to haunt.

JB how about a link to the standard of care you state, or a link to your protocol that gives IN glucagon administration.

I've worked in several places that used IN for many drugs, but none used it for Glucagon.

Edited April 6, 2011 by island emt

[BEorP]

Man, great responses.

I'm glad others have chimed in to defend protocols, as I have no general disrespect for protocols but find that patients often don't fit nicely into any one protocol.

Example. 80ish female, known diabetic, CVA x 2 within the last year each leaving pt with deficits, bedridden x 2 years. Called for 'unresponsive.' U/A pt is laying propped up on pillows in soaking wet bed clothes secondary to diaphoresis, arms clamped tightly to chest, a puddle of drool on her chest, very thin even when age is considered, BGL 27, unresponsive, airway patent, very obvious R sided facial droop not present when she went to bed last night and it's 'believed' that her face appeared normal when checked on two hours previous by daughter, PERRL, skin turgor very poor with significant tenting.

Hopefully without trying to go through the entire presentation I'm making it clear that my initial impression was likely hypoglycemia/possible CVA. Fire is on scene, has Glucagon/syringe layed out on the bed for me. When I try to straighten her arms to check for IV sites I get a nauseating grinding in the elbow/shoulder joints bilat...I've not really felt anything like it before but it concerned me that I may damage her if I apply any firm pressure to straighten them. Access very poor due to dehydration. I make one attempt on the back of her forearm and miss, my partner makes two attempts in her legs, neg x 2. We are both competent when starting IVs.

I decide to start an IO, (pissing of Fire with my 'cowboy shit'), as I don't want to wait on the Glucagon to work before deciding if I'm going to alert the stroke team secondary to the facial droop. I'm also not confident that the Glucagon will create a significant benefit for a patient in this condition that may not have sufficient glycogen stores. Also, I don't want to complicate her in hospital care by burning up any glycogen she may posses if I have an option, thus the I/O.

Now, this is where we have to think, in my opinion. Protocol says that hypoglycemia with 2 or more IV attempts and access unlikely to give Glucagon. But the protocol is unaware that my patient may also be having a stroke. Stroke protocol says that if the patient is positive for Cin stroke scale to activate stroke team (after gathering competent history of course) and transport L/S to appropriate center. But the protocol doesn't know that I am unable to do a neurological assessment secondary to hypoglycemia.

So I set my I/O, push some Lidocain and sugar, pt wakes up, straightens up, face goes back where it belongs, stroke scale negative, transport is uneventful. I believe that I have helped the patient, I am way ahead of the game had the stroke scale been positive. I feel good, the patient is doing well, I'm proud of this call.

Yet it's one of three calls that they cited when they terminated me. Their argument was that it was "too aggressive and outside of protocol. You just don't start an I/O for hypoglycemia!!" For the record, my protocol for an I/O at the time was at least two missed IV attempts with IV access unlikely but access appears necessary. For Glucagon at least two missed IV attempts when access appears "impossible." I explained that we made three attempts without the likelihood of success with future attempts. And that I didn't use the Glucagon as access wasn't impossible, as proved by my successful I/O placement." I don't believe that there was one single 'cowboy' moment here. But my employer felt differently.

So, I went on my way, now work for a really cool company, doing really cool stuff, and life goes on.

So, hopefully this shows that I have no disdain for protocols or guidelines, only that they often, maybe even rarely, address more than one condition at a time and my experience has been that medical patients rarely, and trauma patients seldom, present with a single issue. 95+% of the time these issues can be resolved without any 'cowboy' shit, but sometimes, in my opinion, you are forced to decide your loyalties...to your patient, or the powers that be?

Great thread all! Thanks for taking the time to participate..

Dwayne

Edited to correct a grammatical error only.

Dwayne, sorry if I missed this somewhere with all of the "distractions" that made their way into the thread, but let's just say that this lady was having another CVA and you got her sugar up and alerted the team. Would she actually have had any real chance of receiving tPA? Based on the overall heath you describe along with bystanders not being sure she was seen in her usual state of health recently would make me think that no doc where I brought stroke patients would give much thought to tPAing her.

Since the glucagon was already out, did you consider administering that and then following up with dextrose once you obtained some type of access?

[Richard B the EMT]

As per the US National Library of Medicine, National Institutes of Health,

]

Endocrine IndexGlossary

Glucagon

Glucagon has a major role in maintaining normal concentrations of glucose in blood, and is often described as having the opposite effect of insulin. That is, glucagon has the effect of increasing blood glucose levels.

Glucagon is a linear peptide of 29 amino acids. Its primary sequence is almost perfectly conserved among vertebrates, and it is structurally related to the secretin family of peptide hormones. Glucagon is synthesized as proglucagon and proteolytically processed to yield glucagon within alpha cells of the pancreatic islets. Proglucagon is also expressed within the intestinal tract, where it is processed not into glucagon, but to a family of glucagon-like peptides (enteroglucagon).

Physiologic Effects of Glucagon

The major effect of glucagon is to stimulate an increase in blood concentration of glucose. As discussed previously, the brain in particular has an absolute dependence on glucose as a fuel, because neurons cannot utilize alternative energy sources like fatty acids to any significant extent. When blood levels of glucose begin to fall below the normal range, it is imperative to find and pump additional glucose into blood. Glucagon exerts control over two pivotal metabolic pathways within the liver, leading that organ to dispense glucose to the rest of the body:

• Glucagon stimulates breakdown of glycogen stored in the liver. When blood glucose levels are high, large amounts of glucose are taken up by the liver. Under the influence of insulin, much of this glucose is stored in the form of glycogen. Later, when blood glucose levels begin to fall, glucagon is secreted and acts on hepatocytes to activate the enzymes that depolymerize glycogen and release glucose.
• Glucagon activates hepatic gluconeogenesis. Gluconeogenesis is the pathway by which non-hexose substrates such as amino acids are converted to glucose. As such, it provides another source of glucose for blood. This is especially important in animals like cats and sheep that don't absorb much if any glucose from the intestine - in these species, activation of gluconeogenic enzymes is the chief mechanism by which glucagon does its job.

Glucagon also appears to have a minor effect of enhancing lipolysis of triglyceride in adipose tissue, which could be viewed as an addition means of conserving blood glucose by providing fatty acid fuel to most cells.


Control of Glucagon Secretion
Knowing that glucagon's major effect is to increase blood glucose levels, it makes sense that glucagon is secreted in response to hypoglycemia or low blood concentrations of glucose.

Two other conditions are known to trigger glucagon secretion:

• Elevated blood levels of amino acids, as would be seen after consumption of a protein-rich meal: In this situation, glucagon would foster conversion of excess amino acids to glucose by enhancing gluconeogenesis. Since high blood levels of amino acids also stimulate insulin release, this would be a situation in which both insulin and glucagon are active.
• Exercise: In this case, it is not clear whether the actual stimulus is exercise per se, or the accompanying exercise-induced depletion of glucose.

In terms of negative control, glucagon secretion is inhibited by high levels of blood glucose. It is not clear whether this reflects a direct effect of glucose on the alpha cell, or perhaps an effect of insulin, which is known to dampen glucagon release. Another hormone well known to inhibit glucagon secretion is somatostatin.

Disease States

Diseases associated with excessively high or low secretion of glucagon are rare. Cancers of alpha cells (glucagonomas) are one situation known to cause excessive glucagon secretion. These tumors typically lead to a wasting syndrome and, interestingly, rash and other skin lesions.

Although insulin deficiency is clearly the major defect in type 1 diabetes mellitus, there is considerable evidence that aberrant secretion of glucagon contributes to the metabolic derangements seen in this important disease. For example, many diabetic patients with hyperglycemia also have elevated blood concentrations of glucagon, but glucagon secretion is normally suppressed by elevated levels of blood glucose.

Index of: The Endocrine PancreasPhysiologic Effects of InsulinIntroduction and IndexLast updated on June 15, 1999Author: R. BowenSend comments via form or email to rbowen@colostate.eduEndocrine IndexGlossary