DIP Episode 452 - NMS and Malignant Hyperthermia (vs Serotonin Syndrome)

Welcome, my name is Divine, this episode 452 of Divine Intervention Podcasts. Into this podcast I want to talk about your electric malignant syndrome, malignant hypothermia, and then compare and contrast those with serotonin syndrome. So we're going to go ahead and start with the veneer. So whatever they give you a question about a patient, they tell you that this patient is a 32 year old male, comes into the emergency room because he has been altered or is wife or whatever brings him in because he's been altered. And he has very severe muscle rigidity and you check his lab, he has a lactic acidosis and his crash and burning. And he tell you that he has a pass history of a brain tumor that was found when he presented with erectile dysfunctional low libido and it was placed on pharmacotherapy. And then he was lost to follow up and stopped taking his medication forgot to refill his prescription. So he didn't take his medication for like a week or two and then now he's presenting with these symptoms. What's your diagnosis? Well, this is going to be neuro-eliptic malignant syndrome, NMS, NMS, NMS, NMS. So let's kind of analyze some of the facts of this case. So first things first, this person had a brain mass that killed his libido caused erectile dysfunction. That's probably going to be a prolectinoma. Prolectinoma is remember, they sacred a lot of prolectin and that's going to shut down G and RH. So your HVG axis is basically going to be gone.

You're going to have a hypo-gonadotropic hypo-gonadism. Hypo-gonadotropic hypo-gonadism. That's very important to kind of keep in mind. So that's one. So that's why the person has the low libido and the erectile dysfunction. And sometimes people can have visual problems. They'll have a bite temporal hemianopsy because that prolectinoma can compress the optic chiasm, just one of those rare things to keep in mind. So how in the world do we treat prolectinomins? We're going to treat prolectinomins by giving a dopamine agonist because dopamine can inhibit the production of prolactin. And many times it controls those people's symptoms. So you treat it with dopamine agonist like brymocryptinocarbagolid. But you need to make sure that that dopamine agonist is taking consistently. And when you're withdrawing the dopamine agonist, you need to do it wisely. If you are properly stop a dopamine agonist, that can cause neuroelptic malignant syndrome, especially ins susceptible individuals, especially ins susceptible individuals. Many people don't think about this. They think of NMS as something you only get when you take an anti-psychotic, which is probably the more common scenario. So when you take an anti-psychotic like calopyridol or something for the has anti-psychotic properties, but using photo-proposes like metoclopromide, which is used for diabetes, gastroparesis, all those D2 blockers. Yes, that can cause NMS.

But one other thing that can cause NMS is when you are properly withdraw a dopamine agonist. So it can give you a question about a person that has Parkinson's disease that develops NMS because for a few days, for whatever bizarre reason, stop taking the adeptinocarbagolid liver-dubacarbitopa, just going to keep that stuff at the back of your mind. That's very, very important. That's another pathway to developing NMS. So NMS, what do we typically do to treat NMS? Well, typically we do a few things. Many times you can try to give the person, dantrolling. Dantrolling is a ryanodine receptor antagonist. It prevents you from releasing calcium from the sacroplasmic reticulum so that you don't have that hypercontractile muscle state. And then in addition to that, you can also try to cool them down. Many times you can give them benzos if they are very agitated to calm them down as well. And in some situations, if you don't see any of those answers, consider giving a dopamine agonist because many of these problems come from D2 blockade. So if you give a dopamine agonist like bromocryptin, for example, it will be helpful to these people. So let's compare and contrast NMS to malignant hypothermia. The presentation is pretty similar in general. The only problem is that malignant hypothermia, the exposure, the thing that causes the problem is different. So we said NMS, you get it by either being exposed to a D2 blocker, anti-psychotic, basically, including the typical anti-psychotics.

Or you withdraw a dopamine agonist. Malignant hypothermia, typically, it happens in people that are susceptible, people that have a genetic susceptibility that are exposed to certain kinds of volatile anesthetics or the depolarizing your muscular blocking drugs. So volatile anesthetics, what are some of them? There's going to be things, many of them ending in the end of fluorine, right? So things like halothane, syvophluorane, desfluorane, isofluorane, endfluorane, right? And then the depolarizing your muscular blocking drugs like succinocholine, those ones are the things that typically trigger that problem. So malignant hypothermia, typically, the genetic mutation that causes that problem is when you have a mutation in the ryanodine receptor, the ryanodine receptor, the ryanodine receptor, the ryanodine receptor is a calcium channel. We find it on the sacroplastic reticulum. And when it's activated, it opens up and calcium is then released, increased, released from the sacroplastic reticulum for your muscles to contract. But when it's mutated, especially in the A site, it's a calcium channel, it has an A site and an eyesight. And eyesight, I believe that's for activation, eyesight, I believe that's for inhibition to cause it to close. That eyesight, when it's active, when, you know, people are like, you know, you can have many different mutations that can cause this problem, but generally using the ryanodine receptor and it's inherited in an autosomodominin fascia.

When that happens, you're going to cause crazy, crazy, crazy release of a lot of calcium from the sacroplastic reticulum. So that's going to get your muscles into a hyper contractile state. And as your muscles get into a hyper contractile state, you're going to notice that those people are going to have fevers because they're generating so much heat. They're going to develop a lactic acid dose, think of it like if you're working out, you're going to release a lot of lactic acid from, you know, all that metabolism. And also, as those muscles cells begin to die, then they can begin to spill their content into the bloodstream, like myoglobin. That myoglobin can go to the kidneys and cause rhodomalysis. As your muscles cells are exploding, the intracellular ion potassium is going to be released. That can cause hyper-calemia. That can cause EKG abnormalities like premature ventricular complexes and things like that. Also these people, they can release phosphates. Remember, muscles contain ton of phosphate. They can release into the bloodstream. They can have hyper-phosphatemia. Remember phosphate loves to bind calcium so you can clobber down the acerome calcium levels. They can have high pool calcium. So they can have many, many problems. They can have many, many problems, many, many problems. So you're just going to keep this at the back of your mind.

And again, since the problem is in the rhododium receptor, it will make sense that if you give a rhododium receptor antagonist, like dantrullin, that can really help in situations like this. That can cause a rhododium receptor antagonist. So again, at many times, if a person is, you know, if you notice that once a person has a family history or a person has had a bad reaction to anesthesia, you're probably going to want to want either not to use these agents in these people, these agents I mentioned. But two, you should also do some kind of genetic testing. Anytime you can do a muscle biopsy, it's very, very sensitive for diagnosis, malignant hyper-hyperthermia. That's just something you want to keep at the back of your mind for, for example. Okay? So remember, malignant hyperthermia, these people are going to have fever. You're going to see muscle rigidity. And then you're going to see many antioxidants over robbed myoluses, things like hyper-calemia, hypocalcemia, hyper-phosphatemia. You're going to see the acute kidney injury from all those problems. But in general, there's nothing that happens with the reflexes in people that have malignant hyperthermia. That's a very critical difference between malignant hyperthermia and serotonin syndrome. Serotonin syndrome, those people are going to have some kind of hyper-kinesis. They're going to have increased deep tendon reflexes. They're going to have hyper-reflexia versus people that have malignant hyperthermia.

They tend to be more hypokinetic. They don't move as much. So it's just something that I think may be very helpful to keep in mind for, for exams. And again, the way you treat malignant hyperthermia is exactly the way you treat an MS. For the most part, although malignant hyperthermia, the definitive antidote is dantrulling. Again, it decreases the release of calcium from the cephalplastic reticulum. Okay? So just make sure you can compare and contrast these things. Make sure you have that understanding. I think it's something that will be very helpful to you to, you know, getting these questions right on exams. And they love, love, love, love to test the stuff. So it's just something you don't want to completely forget because again, there's probably going to be some steep price that you pay in those circumstances. Okay, so I'm going to go ahead and pause here as I do. This is probably one of my shorter podcasts because again, I just want to do this versus that. So I can just truly understand these things. As I do at the interview broadcast, I offer one or one to your info, step one to three. Very clean, cool med school exams, 30-ish-off exams, I have a review courses. That's what I do most of the time for people. I'm able to find it to be really, really helpful. So review courses for step one, for step two and step three, for biostatistics, social sciences, ethics, quality improvement and whatnot. And I also have a very heavily acclaimed MDME testing and strategy scores.

If you're interested in any of these courses, just shoot me an email through the website and also have podcasts that I've made on those. So I also have these podcasts on Apple Podcasts Google Podcasts on Spotify. I have a You Tube channel, Divine Intervention, USMLE podcast and videos where you can check some of my videos out. And then finally, I also have a new website called Divine Intervention Lifelesses.com. It's a Bible-based website and every week I post two podcasts that address a life lesson from a biblical perspective. There is an Apple Podcast associated with it called the Divine Intervention Life Lessons Podcast. If you're interested, just check it out. I think you're going to find it to be helpful. Well, thank you for listening to me today. Until next time, have a wonderful week. God bless you.

Withdrawal from dopamine agonists (used to treat prolactinomas).

D2 receptor blockers (e.g., antipsychotics, metoclopramide) or withdrawal of dopamine agonists.

Mutation in the ryanodine receptor, which controls calcium release from the sarcoplasmic reticulum.

Volatile anesthetics ending in -fluoro (e.g., halothane) and depolarizing muscle relaxants (e.g., succinylcholine).

MH tends to be hypokinetic/normal; SS tends to be hyperreflexic/increased DT Rs.

Optic chiasm, leading to bitemporal hemianopsia.

It is a ryanodine receptor antagonist that prevents excessive calcium release from the sarcoplasmic reticulum.

The GnRH/Gonadal Axis (leading to hypo-gonadotropic hypogonadism).

Rhabdomyolysis (myoglobinuria), hyperkalemia, and hyperphosphatemia.

Phosphate is released from damaged muscle cells and binds with calcium, potentially causing hypocalcemia.

Mutation in the ryanodine receptor gene (inherited autosomally dominant).

Dopamine agonists (e.g., Bromocriptine).

It is a ryanodine receptor antagonist that prevents excessive calcium release from the sarcoplasmic reticulum.

The GnRH/Gonadal Axis (leading to hypo-gonadotropic hypogonadism).

Rhabdomyolysis (myoglobinuria), hyperkalemia, and hyperphosphatemia.

Phosphate is released from damaged muscle cells and binds with calcium, potentially causing hypocalcemia.

Mutation in the ryanodine receptor gene (inherited autosomally dominant).

Dopamine agonists (e.g., Bromocriptine).