false
Catalog
SCCM Resource Library
Not Too Sweet or Salty: Glucose and Sodium Homeost ...
Not Too Sweet or Salty: Glucose and Sodium Homeostasis
Back to course
[Please upgrade your browser to play this video content]
Video Transcription
All right. And to close this out, we're going to talk about, essentially, sugar and salt and try to fit it into a 15-minute time frame, which is going to be challenging. So I'll try to talk fast. So hyperglycemia, I don't think it's a surprise to anybody that this occurs. And the reason is simple. It's the stress response that's been well-detailed in some of the other talks. So endogenous catecholamines, cortisol, and it starts this inflammatory response. Also, not surprisingly, it's bad for the brain. And so typically, this is, again, because of this continuous inflammation that occurs that leads to cell death. There's also consideration that there's an increase in glutamate, which can worsen cerebral ischemia. So in the disorders that we see often when we're talking about the injured brain, there are specific consequences to hyperglycemia. In stroke, it increases metabolic demand, causes neuronal death, breaks down the blood-brain barrier, potentiates endothelial dysfunction, impairs fibrinolysis. Actually, it's predictive. If somebody is going to have hemorrhagic transformation or not, it can cause an expansion of infarction. It's associated with cerebral edema, and it can cause disability and death. In TBI, this has also been fairly well studied. Levels greater than 200, and that's just a one time greater than 200, are associated with a 2.6-fold increase in in-hospital mortality. So a big deal. And unsurprisingly, increases disability and death. In ICH, associated with hematoma expansion, perihematoma edema, blood-brain barrier disruption, and this is, again, going to shock you, disability and death. And then lastly, in subarachnoid hemorrhage, associated with spasm, systemic complications, and then disability and death. So we should probably aggressively treat this, but we actually found that our previous guidelines of 80 to 110, based upon the Nice, Sugar, and Shine studies which admittedly were adult trials, that this actually caused more harm due to hypoglycemic events, so we've shifted to this accepted 140 to 180 range. So on the other end of this, hypoglycemia, also bad for the brain. It's usually iatrogenic, it's something that we do. We give a bunch of insulin, and then for some reason we take away exogenous sources of glucose, but we know there are other etiologies, such as sepsis or systemic issues. We know that in a healthy brain, you need 20 to 25% of your glucose supply. There's a marked increase in this in patients that have brain injuries, so it becomes even more important. And this can cause an alteration of cerebral blood flow, impaired metabolic function, and again, just overall bad for the brain. Treatment is very simple. I think you guys can guess what it is. If you don't have enough, then you give a little bit more. So sodium disorders, this alone could probably be an hour discussion, so we'll see how we do. So hypernatremia, when we're seeing this, most of the time it's because we've given hypertonic saline to reach a certain goal, decrease herniation, impending herniation, or cerebral edema. And DI, we're gonna talk more specifically about. So it was already alluded to that this is a disorder of reduced AVP because of the HPA or the pituitary axis and the effect of brain injury on that. So what this means is you have increased free water loss and that causes hypernatremia. And so this presents as polyuria, polydipsia in patients that are able to express that, which is typically not the organ donation population, and a rise in sodium that should trigger workup for this. And so these patients have a large volume of dilute urine, and then again, the rise in sodium. Causes, really anything that is going to cause brain injury, so TBI, pituitary tumors, or whether you have surgery, you have an anterior communicating artery aneurysm or subarachnoid hemorrhage that's centered in that area. Anoxic brain injury, really any diffused disorder that could cause a herniation syndrome. Again, as mentioned, this is associated with severe cerebral edemia and impending death. And often this comes before formal brain death, though it doesn't always have to. In terms of labs that you might get, you'll be looking at serum and urine osmos, serum sodium, urine-specific gravities. And so if you have an increased sodium and serum osmo and decreased urine osmo with a spec grav typically less than 1.005, you would consider that consistent with DEI. So treatment, again, if you don't have enough of something, then you're going to supplement it. So you're gonna give exogenous AVP. There are a lot of different routes that we can accomplish this with. If it's somebody that has come in for a simple pituitary tumor resection and is not in the ICU, that would be somebody you'd consider enteral augmentation. That's not gonna be the case with the patients that we're seeing in the ICU. You can give IV or sub-Q in divided doses, and you're looking for that goal urine output of 0.5 to three mils per kg per hour. But if a patient's hemodynamically unstable, that's when you would consider a continuous infusion of vasopressin, titrating for that goal. And you're gonna see, I have nursing considerations kind of sprinkled through this, and they're gonna be very, very similar for all of this, which is we're gonna be following a close exam. Really strict I's and O's, not one of those every four hours, I'm gonna dump it and divide by four. We need to know every hour or every two hours what's happening, that you might be doing aggressive volume replacement to maintain uvulemia. So if somebody says to give a high volume, you're not gonna spread that out. You need to make sure that you have good access and follow it, and that labs also need to be performed in a timely manner. So on the other end of that spectrum, these are gonna be hyponatremic disorders, and it's really, really important to distinguish between these two that we see frequently, which is cerebral salt wasting versus SIADH. I'm actually gonna start with SIADH because it's kind of the opposite of DI. So in this case, you now have too much AVP, and with that, you have increased free water resorption and a dilutional hyponatremia. But these patients never actually look super overloaded. The etiology is vast, and it can occur, again, with just about any CNS disorder, including getting into CNS infection, and can be a complication of certain medications. And remember, hyponatremia is the most common electrolyte abnormality that you actually see in the hospital, so it's important to differentiate. So water will shift from the extracellular into the intracellular, and when this happens, the brain, since it's already injured, can't counterregulate the way that it normally would. And with this, you can actually cause herniation and see an increase in ICP. Often, it's a diagnosis of exclusion, so you're gonna wanna make sure that there aren't adrenal or thyroid abnormalities before you settle on it. But features can include hyponatremia, a low plasma osmo, increased concentrated urine, an increased urine sodium, and typically, this looks like a uvolemic disorder. And you'll see that figuring out fluid balance is going to be paramount to doing this. There's also something that's a little specific to the PEDS population that hasn't been well-researched in the adult population when differentiating between the two disorders, which is looking at serum aldosterone. So in SIDH, in the pediatric population, you have an increase of serum aldosterone, wherein cerebral salt wasting, you actually have a decrease, as well as suppressed plasma renin activity, which will be interesting if anybody tries to extrapolate that to adults later on. So treatment kinda depends on what's going on with the patient. If this is somebody that's a coma, seizing sodium less than 120, then obviously you're going to more aggressively augment until you see an improvement in symptoms. Still trying to keep in mind that eight to 10 mL equivalents per 24 hours, 18 over 48. And so the reason that you do that is you're trying to prevent osmotic demyelination, which is like an irreversible paralysis that can look like a locked-in syndrome. In patients that are more moderate, that they have more subtle symptoms, like confusion, nausea, you could give small boluses of hypertonic to try to get them up, but you're gonna focus on fluid restriction, and in minor symptoms, again, not the organ donation population, you're just gonna restrict fluids. Now, if you start to move too fast, you can consider giving a little dose of DD-AVP, and then starting to actually give free water back to prevent that rapid shift, because as much as we'd like to predict how every patient is going to react to fluid restriction and hypertonic, we can't necessarily do so reliably. So just watch that. And shockingly, the nursing considerations are gonna be the same. Follow the exam, strict I's and O's, get the labs as quickly as we actually need to get them, and to ensure that our fluid balances are where we want them. So cerebral salt wasting is a little bit different, and we're kind of moving a little away from AVP. It's excess renal excretion of sodium and water, and the exact reason isn't known. This is one of those, well, we think it's because of this, but the thought is that it's because of a neuroendocrine disruption that causes an increase in BNP, and decreased sympathetic tone that causes this excess loss of water and sodium. And so these patients are dehydrated. So again, that's one of the big differences to know. These are patients that are gonna look hypovolemic, which is super dangerous in the population of aneurysmal subarachnoid hemorrhage specifically. So treatment for this. Again, frank hyponatremia means you need to correct it very similarly to how we would actually correct it with SIDH, except you're not restricting fluid now. You wanna maintain uvulemia. Fluid or cortisone can be considered in patients that don't have a sustained response that you're looking for with augmented saline with hypertonic solutions. Very surprisingly, we're gonna look at nursing telling us about exam, eyes and nose, labs, vital signs. Something else to consider is that if somebody is on fluid or cortisone, they might also need potassium supplementation. And so this is our nice little snapshot that says everything that I said in 30 seconds instead of 15 minutes. And then what's the effect on organ viability? So interestingly, with hyperglycemia, there haven't actually been studies that have shown that more aggressive and tight control of glucose in the donor has any effect on graft function. I'm sure hypoglycemia would be a little bit different, but hyperglycemia is relatively well-tolerated in the transplant recipient. Now, hypernatremia is very, very different, and it's associated with delayed graft function and actually complete graft loss. And the hypothesis for this is that there's increased edema, and so when you're doing your anastomosis, that you can have vessels that aren't quite connecting the way that you would want, and swelling that occurs that decreases your flow through. And so when you're making those connections, you're actually decreasing blood flow to the transplanted organ. And so a lot of centers have cutoffs in terms of when they'll utilize these organs. I know at Mayo, and I do work on the transplant side there, for brain death, we'll tolerate a little bit more and go to sodiums of 160. But if you're doing a DCD, we limit at 155, and that's because of what we found with graft function. And actually, that wasn't too bad. All right, thank you so much.
Video Summary
This video discusses the impact of sugar and salt on the brain in various brain injuries, such as stroke, traumatic brain injury, intracerebral hemorrhage, and subarachnoid hemorrhage. Hyperglycemia (high blood sugar) can increase metabolic demand, cause cell death, impair brain function, and lead to disability and death. Hypoglycemia (low blood sugar) can also be harmful and should be treated with glucose supplementation. Hypernatremia (high blood sodium) can cause cerebral edema and increase the risk of disability and death. On the other hand, hyponatremia (low blood sodium) can result from either cerebral salt wasting or SIADH, both of which require careful management and fluid balance monitoring.
Asset Subtitle
Pharmacology, Endocrine, 2023
Asset Caption
Type: one-hour concurrent | The Endocrine System Must Live on in Severe CNS Illness and Injury (Pediatrics) (SessionID 1220102)
Meta Tag
Content Type
Presentation
Knowledge Area
Pharmacology
Knowledge Area
Endocrine
Membership Level
Professional
Membership Level
Select
Tag
Fluids Resuscitation Management
Year
2023
Keywords
sugar impact on brain
salt impact on brain
brain injuries
hyperglycemia
hypernatremia
Society of Critical Care Medicine
500 Midway Drive
Mount Prospect,
IL 60056 USA
Phone: +1 847 827-6888
Fax: +1 847 439-7226
Email:
support@sccm.org
Contact Us
About SCCM
Newsroom
Advertising & Sponsorship
DONATE
MySCCM
LearnICU
Patients & Families
Surviving Sepsis Campaign
Critical Care Societies Collaborative
GET OUR NEWSLETTER
© Society of Critical Care Medicine. All rights reserved. |
Privacy Statement
|
Terms & Conditions
The Society of Critical Care Medicine, SCCM, and Critical Care Congress are registered trademarks of the Society of Critical Care Medicine.
×
Please select your language
1
English