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Let's talk about anaphylaxis and let's go a little bit into the past. And you say, why do we even talk about the past? Because the past is the future. Where'd the term come from? Now, back in 1902, when vaccines were first being experimented on, Charles Richard and Paul Portier base experiments attended to immunize dogs against toxins from Mediterranean sea anemones. And this is going to be to for creating vaccines for humans. This was the first step. And they were injecting this toxin into dogs. And this was the beginning of vaccines. And they were trying different ways to create vaccines. Whoever the dogs died. They had wheezing, vomiting, and then died. And so they named this is anna equal phylaxis. Anna equals absence plus phylaxis protection, anti-protection, because they're trying to come up with protection and vaccine. I know you said that's not important. It is important. The past is the future in medicine. Let's talk about mechanisms of anaphylactic activation. Remember, anaphylaxis is a severe inflammatory response caused by rapid activation of mast cells and basophils. The activation release mediators, you had two routes. The classic, here it is, the IgE-mediated pathway. This is the classic. And then there's the non-Igmated pathway. This is the alternative way. So in the IgA, you have prior sensitization and IgE binding. And it binds on the receptors on the mast cells and basophils. Then you have an allergen cross-reaction. And it triggers allergen to binding to the IgE, causing cell degranulation and mediator release. In the non-IgE mediated pathway, it's receptor-driven activation. The IgG immune complexes can trigger degranulation without IgE involvement. There's complement system activation and directly stimulates mast cells through specific surface receptors. Now, what happens is what's your response is you have histamine, tryptinase, leucotrians, and prosaglandins. Rapid release of preformed histamine, tryptinase, plus newly synthesized leucotrians and prosyglanins. Now certain medications, exercise, even cold temperatures can stimulate mediator release. Let's get a better understanding of anaphylaxis, the mechanisms and clonal diagnosis. Anaphlaxis is a rapid systemic reaction driven by inflammatory mediators like histamine and tryptase. So let's talk the pathophysiology and internal mechanics. You have mediator-induced vascular response. Histamine increases capillary permeability and increases vasodilation, leading to fluid extravization and hypotension. What's another thing we see in medicine that can do that? Gram-negative sepsis causes that rapid vasodilation, which leads to hypotension. You get the blood pulling in the peripheral and you have to squeeze it up, squeeze it up into the core. You have response amplification and signaling. Tryptase stimulates further mass cell degranulation, and then neuronal signaling propagates response to distant sites. So we have a systemic response. We don't have a localized, we have a systemic respiratory and organ impact. Leucotrians drive bronchoconstriction. Remember, we want bronchodilation in a lot of these cases, potentially resulting in cardiovascular collapse andor asphyxiation from away edema. What are some clinical manifestations and diagnosis? The highly likely is that the diagnostic rule, acute skin mucosal involvement paired with either respiratory compromise or sudden hypotension. This is very highly likely. There's no test. There's no test that says, he's an anaphylaxis. No, there's no test. Is you have acute skin mucosal involvement. Now, mucosal can also be what are other areas we have mucosal? In our groin is a mucosal area. All right, so acute skin and mucosal, mouth groin, those areas. And we either have respiratory compromise or sudden hypotension. We have multi-organ system involvement. Rapid diagnosis is warranted. You don't have to, oh, let's get a test for anaphylaxis. No, you need to act quickly. Rapid diagnosis is warranted when two or more organ systems react after allergen exposure. Life-threatening features, critical signs include laryngeal spelling. Remember, we talked about mucosal involvement, hypotensive shock, cardiac arrest, or severe bronchospasm, or all the above. All the above. So let's talk about the diagnostic pathways. Require clinical evidence. Pathway one, acute skin, mucosal onset, plus rapid respiratory compromise or hypotension. Pathway two involves two or more organ systems rapidly after exposure. So they could be blood pressure and breathing, could be the lungs and breathing, hypotension occurring after exposure to a known antigen for that patient. Or it could be unknown. You could say it's unknown because you're not going to have time. Sir, are you having an allergic reaction right now? No, these are not discussions you're going to be having. Let's talk about the clinical foundations, diagnosing anaphylaxis. Primary diagnostic criteria. Why do we go over this twice? Because you need to know this. This needs to be burned in your brain so you activate rapidly. See how this guy's running? This shouldn't you be running for a treatment? And we'll talk what that treatment is. And you shouldn't be going, well, I wish I could get a lamp test. Are you in anaphylaxis? No, you're going to work on this. Criteria one, skin plus systemic involvement. You have skin mucosal issues combined with respiratory hypotension or GI symptoms. Note two. Criteria two, known allergen exposure. Now you can also say unknown because these are times you're not going to be able to react. And patients going, yes, I'm having anaphylaxis right now. No, they're going to be on the verge of dying. Acute respiratory or cardiovascular symptoms occurring even without skin or mucosal involvement. You're not going to be sitting in the lawyer's office going, you know, they didn't tell me they're having anaphylaxis when they were having trouble breathing or were hypertensive with mucosal involvement. No, you're not going to be able to do that. You're going to have to act rapidly. Rapid detection windows onset occurs within minutes. The reaction can manifest itself up to 10 hours later. Critical risk factors and indicators, high mortality risk systems. Symptoms involve laryngeal, respiratory, or cardiovascular symptoms leading to the highest risk of death. Just think about it. If you're not breathing, you're not doing well.

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Okay.

SPEAKER_00 6:51

If you're not breathing, and if you're not breathing, you're going to say, I'm having anaphylaxis right now. Non-food GI call clues. Severe abdominal pain or vomiting is highly indicative of after non-food allergen exposure. Makes sense, right? The body's just going, I am not tolerating this. I am going to shut down. Limitations of clinical tools. Diagnostic is purely clinical. That's why we're burning this into your brain. This is so important. You take care of these patients. These are important patients you take care of because if you miss this, they die. No laboratory findings or epinephrine response confirms it. So you can't say, I gave the epinephrine, they had anaphylaxis. So you have to use your brain. Let's talk about emergency management of anaphylaxis, the critical protocol. Well, the critical protocol is you give epinephrine. I am is a standard of care. Now there is internasal applicators that can be used, and some people have those and carry those around instead of a standard uh auto-inject pen. And they can be used, but the standard of care is IM. So you're going to give IM. Immediately administer epinephrine IM. You're going to inject 0.3 to 0.5 milligrams IM every five to 15 minutes as the primary standard of care. Primary standard of care. And if they're still having symptoms, you start them on an epinephrine drip. Epinephrine drip. You're going to optimize patient positioning. Now, normally you would lay them recombinant with their legs elevated because when you raise their legs, raise their legs, is you're going to perfuse to the core about three 200 to 300 milliliters of blood coming from the legs to the core. Because remember, we're trying to what? Protect our map. We're trying to protect the core, the main organs. We're trying to perfuse those. Now, in this case, this patient was vomiting. Remember, we said that some people can be vomiting, so we're trying to protect their airway. So there can be different ways to optimize patient positioning. Now, if the patient's not nauseous and protecting their airway, you can lay them on their back and put their legs up. You can give rapid fluid infusion, okay? You want to give that resuscitation to get those pressures up. Now you can also use albuterol for respiratory distress. Remember, some people are going to be wheezing, and or glucagon for patients who are taking beta blockers because they may blunt the response of the epinephrine. So beta blockers can blunt the response of epinephrine, and you would give glucagon. Now, these other therapies, and I know a lot of people give these first, but they're not clinically proven to make the change. This is what's going to save someone's life is the epinephrine. This is going to change the world for them. This is, we'll call it window dressing. And if you want to use this for symptoms for the patient after you taking care of the major things, if they're not breathing, none of this matters, right? So secondary therapies, antihistamines, and steroids are not routine, only used for persistent cutaneous symptoms. So basically, you stabilize this patient, then you can use these. And you need to have extended clinical observation. Now it says monitor four to eight hours. Some people say because there can be a post-resolution prevent and manage biphasic reactions. Sometimes you have a second reaction with four to eight hours. You can see some literature that will say is monitor them for 12 to 24 hours. That's going to be based off your system. Now, what's really important, really important, is you need to have following this, you need to have patient education. You need to provide them with an epinephrine auto injector and how to use this and show this and how prevention of the treatment for recurrent attack. If it becomes from an unknown source, they're going to need to have immediate appointment with an allergist to figure out where this came from. What they need right away is an epinephrine autoinjector. Now, there is a nasal spray, an epinephrine nasal spray, which is approved for by the FDA for emergency treatment of type 1 allergic reactions, including anaphylaxis. It is an alternative to epinephrine auto injectors. You may find it cheaper. The other thing is that it doesn't expire as fast as the auto injectors. It doesn't expire as that, so it can last longer. So it may be a lower cost overall for the patient. So this is anaphylaxis, it's giving you some clues on anaphylaxis and how to treat it and what you need to do as a provider.