EP1 | Anaphylaxis: Recognition, Pathophysiology & Management
Welcome to the very first episode of MedSimu Emergency Podcast.
Speaker 2:It's great to be starting this.
Speaker 1:Anchor: Yeah, I'm thrilled to be kicking things off with, well, a really critical topic for all of us in emergency medicine. Doesn't matter if you're a seasoned attending or, you know, just starting your medical journey.
Speaker 2:Absolutely.
Speaker 1:Today, we're doing a deep dive into anaphylaxis.
Speaker 2:A big one, and something we see often.
Speaker 1:Exactly, and with me is an expert in the field who's gonna help us unpack this common yet potentially life threatening emergency.
Speaker 2:It's a real pleasure to be here. Anaphylaxis, yeah, it's something we encounter frequently and a thorough understanding is just crucial for timely, effective management.
Speaker 1:Definitely. We'll be drawing from established medical knowledge today trying to really understand the nuts and bolts of anaphylaxis.
Speaker 2:The
Speaker 1:goal is a clear, concise overview for your exam prep, but also for your clinical practice.
Speaker 2:Right, bridging that gap.
Speaker 1:Our mission today is really to cut through the complexities, highlight what truly matters when you're faced with a patient having this acute hypersensitivity reaction.
Speaker 2:Let's do
Speaker 1:it. So to get us started, maybe you could paint a clear picture. What is anaphylaxis fundamentally?
Speaker 2:Okay. So anaphylaxis is this rapidly evolving generalized multi system allergic reaction.
Speaker 1:Multi system. Okay.
Speaker 2:Yeah. And what makes it so critical? So dangerous is its potential to quickly lead to respiratory collapse. It's truly life threatening. It's interesting, you know, historically we used to make this distinction between IgE mediated reactions, the classic allergic ones and others, the IgE independent ones.
Speaker 1:Right. Anaphylactic versus anaphylactoid.
Speaker 2:Exactly. But now the consensus is just to use the single term anaphylaxis for all of them. Much simpler. And really it's because clinically they look the same and importantly we treat them the same. Doesn't matter what kicked it off.
Speaker 1:That makes sense. Focus on the patient, not mechanism initially.
Speaker 2:Precisely. That shift really highlights focusing on the clinical picture right in front of you.
Speaker 1:Okay. So, knowing it's that kind of multi system rapid reaction, what are the typical things we see that, that set it off? The triggers.
Speaker 2:Right. The etiology. Well, there's a range. Common ones are definitely medications, certain foods, and of course insect stings.
Speaker 1:The usual suspects.
Speaker 2:Yeah. But also things like immunotherapy injections, allergy shots. Ironically, they can sometimes cause an acute reaction.
Speaker 1:Okay, good point.
Speaker 2:And we're seeing more latex hypersensitivity which, like any severe allergy, carries that risk. And then sometimes you just don't know. Despite everything, the trigger remains unknown. We call that idiopathic anaphylaxis.
Speaker 1:Frustrating, I bet. So if we had to maybe narrow it down for say a new resident, what are the absolute can't miss triggers they need to have on their radar in the ED?
Speaker 2:Yes, good question. For insects, definitely think bee stings, wasp stings, also fire ant bites down south. Latex, keep that in mind, especially with healthcare exposure or certain patient populations.
Speaker 1:Right.
Speaker 2:Foods, the list is long. But the big ones are peanuts, tree nuts, fish, shellfish, then milk, eggs, wheat.
Speaker 1:Common allergens.
Speaker 2:Yeah, but also things like spelt, rye, barley, soy, even red meat, sometimes sesame.
Speaker 1:Red meat. That's interesting.
Speaker 2:Yes. That ties into alpha gal anaphylaxis. It's often linked to a tick bite, specifically the lone star tick.
Speaker 1:Ah, I've heard of that.
Speaker 2:Yeah, it triggers an IgE response to a sugar molecule found in non primate mammals galactose alpha one three galactose. So they become allergic to red meat sometimes hours after eating it.
Speaker 1:Wow. Delayed reaction too. That must make diagnosis tricky sometimes.
Speaker 2:It certainly can.
Speaker 1:Okay. So it sounds like there are quite a few potential triggers. How common is this overall? Are we seeing a lot of it?
Speaker 2:Well, suggest a lifetime prevalence globally of maybe one percent to three percent. But the worrying thing is the trend seems to be increasing.
Speaker 1:Really? Why do you think that is?
Speaker 2:That's the million dollar question. Theories range from the hygiene hypothesis to changes in diet and environment. But we don't know for sure. It does seem more common in younger people and in developed countries. And a really significant issue is misdiagnosis or under diagnosis.
Speaker 2:Patients might have symptoms, but it's not recognized as anaphylaxis quickly enough.
Speaker 1:Which delays treatment.
Speaker 2:Exactly, leading to increased morbidity and potentially mortality. Timely treatment is just so, so critical.
Speaker 1:Absolutely. Early recognition is key. So, okay, we have these triggers. What's actually happening inside the body? The pathophysiology?
Speaker 1:What leads to such a, well, a dramatic reaction?
Speaker 2:Okay, so typically it's what we call an IgE mediated or type one hypersensitivity reaction.
Speaker 1:Type one. Got it.
Speaker 2:So think of IgE antibodies like little flags already attached to immune cells, mostly mast cells and basophils from a previous exposure.
Speaker 1:Primed and ready.
Speaker 2:Exactly. Then on re exposure to that specific allergen, the allergen binds to these IgE antibodies causing them to cross link on the cell surface.
Speaker 1:Okay.
Speaker 2:This cross linking flips a switch basically. It aggregates these high affinity IgE receptors and triggers the cells to degranulate rapidly releasing a whole cocktail of preformed chemical mediator.
Speaker 1:The bad stuff.
Speaker 2:Well, the stuff that causes the symptoms. Histamine is the big one everyone knows, but also things like tryptase, carboxypythidase A, proteoglycans. And that's not all. This process also kicks off the synthesis of new mediators like arachidonic acid metabolites, leukotrienes, prostaglandins, and platelet activating factor.
Speaker 1:It's a cascade?
Speaker 2:It really is. And TNF alpha, tumor necrosis factor, also plays a role both preformed and produced later in the reaction.
Speaker 1:Wow, okay. That's a lot of chemical players involved. Can you maybe break down what some of key ones do? Histamine, prostaglandins, which ones really drive the immediate clinical picture?
Speaker 2:Sure, let's focus on the big ones. Histamine is a major driver of the immediate symptoms. It causes vasodilation, makes blood vessels leaky and wider.
Speaker 1:Leading to swelling and low blood pressure.
Speaker 2:Exactly. Increased vascular permeability and vasodilation, which drops blood pressure and causes tissue hypoperfusion. The body tries to compensate, so you often get increased heart rate and contractility. Prostaglandin D is another key player. It's a potent bronchoconstrictor, tightens the airways.
Speaker 1:Making it hard to breathe.
Speaker 2:Yes. And it can also constrict arteries in the heart and lungs while contributing to peripheral vasodilation, worsening that hypoperfusion. Double trouble. Pretty much. Then you have leukotrienes, also major bronchoconstrictors increase vascular permeability too, and they might even play a role in longer term airway remodeling.
Speaker 2:Platelet activating factor or PAF does similar things. Bronchoconstriction increased vascular permeability and TNF alpha. It mainly revs up the inflammatory response activating neutrophils, increasing chemokine synthesis, basically calling in more inflammatory troops.
Speaker 1:So it keeps the fire going?
Speaker 2:In a way, yes. It's this complex interplay, but the net result is airway compromise, vasodilation, leaky vessels and potentially cardiovascular collapse.
Speaker 1:Understood. So we've talked about these powerful chemicals getting released just to confirm the underlying cellular event, the root cause is that mast cell and basophil degranulation.
Speaker 2:That's the core event, yes. That rapid degranulation is what unleashes that first wave of mediators and really drives the whole overactive immune response we see clinically.
Speaker 1:Right, okay so now thinking about us on the front lines, what are the key things we need to look for? History, physical exam, what flags should go up that scream anaphylaxis?
Speaker 2:Well, it might start looking like just a mild allergic reaction. You know, some itching, maybe some flushing. The initial symptoms can really depend on the route of exposure. If it was something they ate, you might see respiratory symptoms before prominent skin signs like hives or urticaria.
Speaker 1:Good point. Skin isn't always first.
Speaker 2:No. And you really need to listen for those concerning respiratory symptoms. Things like a feeling of a lump in the throat or persistent throat clearing, difficulty breathing, obviously, hoarseness, any wheezing or stridor that high pitched noise I'm breathing in.
Speaker 1:The stridor is a big warning sign.
Speaker 2:Huge! If any of those respiratory signs are present, need to be thinking immediate intramuscular epinephrine, no delay. Got it.
Speaker 1:How fast does this usually happen?
Speaker 2:It's typically rapid, often within minutes, usually within an hour of exposure.
Speaker 1:Wow.
Speaker 2:And that speed is critical. Sadly, about half of all anaphylaxis related deaths happen within that first hour.
Speaker 1:That really underscores the urgency.
Speaker 2:It absolutely does. Time is everything and generally the faster the onset and the quicker the progression of symptoms, the more severe the reaction is likely to
Speaker 1:be. The
Speaker 2:main killers, the primary causes of morbidity and mortality are loss of airway and that distributive shock we talked about profound vasodilation leading to circulatory collapse.
Speaker 1:Right. Now isn't there something about it coming back like even after they seem better?
Speaker 2:Yes, that's the biphasic reaction. It's really important to remember.
Speaker 1:How common is that?
Speaker 2:It can occur in up to maybe twenty percent of cases. Symptoms recur after initial improvement without any re exposure to the trigger.
Speaker 1:When does that usually happen?
Speaker 2:It typically peaks around eight to eleven hours after the first reaction, but it can be earlier or later.
Speaker 1:And is it usually as bad as the first time?
Speaker 2:It can be. While maybe only four point five percent of biphasic reactions are considered clinically significant or severe, you can't predict it. It could potentially be fatal.
Speaker 1:So that observation period after treatment is crucial?
Speaker 2:Absolutely crucial. You can't just treat and immediately discharge.
Speaker 1:Okay. And beyond the classic airway, breathing, circulation issues, what else should we look for?
Speaker 2:Think about signs of end organ hypoperfusion. Basically organs not getting enough blood flow because of the shock.
Speaker 1:Like what?
Speaker 2:Things like abdominal pain, or cramping, vomiting, sometimes profound weakness or floppiness, hypotonia, fainting or syncope, even incontinence.
Speaker 1:GI symptoms too.
Speaker 2:Yeah, GI symptoms are actually pretty common, maybe in twenty five, thirty percent of patients. So the take home is don't miss anaphylaxis because someone doesn't have textbook throat swelling or wheezing. Look at the whole picture, the timing, multiple systems involved.
Speaker 1:That's a really key point. It's not always the classic presentation. So, okay, suspicion is high. How do we formally make the diagnosis? Are there specific tests we need right away?
Speaker 2:This is critical. The diagnosis is primarily clinical.
Speaker 1:Based on signs and symptoms?
Speaker 2:Exactly. Labs and diagnostics usually aren't needed or helpful for the immediate diagnosis and treatment decision. Speed is everything.
Speaker 1:Don't wait for labs.
Speaker 2:Definitely not. Rapid recognition and action are vital. Remember that first hour fatality statistic.
Speaker 1:Right.
Speaker 2:You should strongly consider anaphylaxis if a patient has involvement of two or more body systems rapidly after a potential exposure, even if they don't have obvious airway compromise or hypotension initially.
Speaker 1:Okay. Are there specific criteria that can help guide us?
Speaker 2:Yes, there are established clinical criteria often attributed to the National Institute of Allergy and Infectious Diseases and the Food Allergy and Anaphylaxis Network. They help standardize diagnosis.
Speaker 1:Can you run through those briefly?
Speaker 2:Sure. There are basically three scenarios that meet the criteria. Anaphylaxis is likely if any one of these is met, usually within minutes to hours.
Speaker 1:Okay. Scenario one.
Speaker 2:Scenario one: Acute onset involving the skin or mucosa like hives, itching, flushing, swollen lips, stung uvula, PLS, either respiratory compromise or reduced blood pressure signs of end organ dysfunction. This applies even if the trigger isn't known.
Speaker 1:Scenario two:
Speaker 2:Exposure to a likely allergen for that patient, A and D, rapid development of symptoms involving ANY two or more of the following systems: Skin mucosa, respiratory compromise, reduced B penned organ dysfunction, or persistent GI symptoms like cramps or vomiting.
Speaker 1:So two systems after a likely exposure.
Speaker 2:Scenario three: Exposure to a known allergen for that patient A and D just reduced blood pressure for their age.
Speaker 1:So known allergen plus hypotension = anaphylaxis
Speaker 2:Pretty much sums it up. These criteria are a great guide but clinical judgment is still key. If you strongly suspect it, treat it. Don't get paralyzed by trying to perfectly match criteria.
Speaker 1:Good advice, what about differentiating it from simple angioedema?
Speaker 2:That's a common question. Angioedema involves swelling often of the face, lips, tongue, airway. It could be part of anaphylaxis or occur on its own like ACE inhibitor induced angioedema. The key difference often highlighted is the presence of urticaria or hives. Hives are typical in anaphylaxis, less so in isolated angioedema, but airway concerns can be similar in both.
Speaker 2:If in doubt, especially with airway symptoms, on the side of caution and treat aggressively as if it could be anaphylaxis. Manage the airway. Think about epinephrine.
Speaker 1:Okay. Mentioned labs aren't usually helpful acutely. What about later maybe for confirmation?
Speaker 2:Yeah, acutely they don't guide immediate management. Serum histamine levels, for example, spike really quickly, but also drop off fast. So they're often normal by the time blood is drawn. Not very useful.
Speaker 1:What about tryptase?
Speaker 2:Serum tryptase is released from mast cells. It stays elevated longer for several hours. So drawing a tryptase level maybe one to two hours after symptom onset can sometimes help confirm that mast cell degranulation occurred.
Speaker 1:That's not perfect.
Speaker 2:No, it has pretty low sensitivity. A normal chip case doesn't rule out anaphylaxis especially in food allergy. So useful if elevated but not definitive if normal. It's more for retrospective confirmation or investigation.
Speaker 1:Got it. And you mentioned Kunis syndrome earlier, the allergic angina.
Speaker 2:Yes, Kunis syndrome. It's essentially an acute coronary syndrome like a heart attack or unstable angina triggered by the allergic or anaphylactic reaction.
Speaker 1:How does that happen?
Speaker 2:Those mediators we talked about like histamine and leukotrienes, can cause coronary artery spasm or contribute to plaque rupture in susceptible individuals.
Speaker 1:So chest pain during anaphylaxis could be cardiac?
Speaker 2:Dr: Absolutely. You need to consider it, especially in patients with risk factors, get an ECG. It's a crucial thing to keep in the back of your mind.
Speaker 1:Okay, fantastic overview of diagnosis. So diagnosis made or strongly suspected, we need to act fast. What are the absolute immediate priorities? The must do steps?
Speaker 2:Right. Treatment. First things first, triage. Any potential allergic reaction needs to be seen urgently. They can deteriorate incredibly fast.
Speaker 2:And then ABC airway is paramount. Assess patency. Look for any signs of impending loss that perirolal edema, the stridor we mentioned, angioedema. These are high risk signs. Prepare for a definitive airway early.
Speaker 2:Delaying intubation while swelling progresses makes it much harder, potentially impossible, increasing the risk you'll need a surgical airway like a cricothyroidotomy.
Speaker 1:Secure the airway first. Okay. What's next?
Speaker 2:After addressing the airway or simultaneously if possible, think about decontamination removing the trigger if you can.
Speaker 1:If
Speaker 2:it was a bee sting carefully remove the stinger without squeezing the venom sac. If it's a medication infusion stop it immediately.
Speaker 1:What about if they swallowed something? Gastroc lavage?
Speaker 2:Generally, no. Gastroc lavage is unlikely to be effective by the time anaphylaxis develops and it just delays definitive treatment like epinephrine. It's not recommended.
Speaker 1:Okay, good to know. Air is secured, trigger removed if possible. Now, the cornerstone medication?
Speaker 2:Epinephrine without a doubt. First line, most important treatment, rapid administration is absolutely key.
Speaker 1:We know the guidelines stress don't delay. Can you maybe emphasize why that speed is so critical? Sometimes there's hesitation, fear of side effects.
Speaker 2:That hesitation can be fatal. Epinephrine directly counteracts the life threatening processes of anaphylaxis. It causes vasoconstriction which raises blood pressure. It reduces mucosal edema helping the airway. It causes bronchopilation opening the airways.
Speaker 2:It stabilizes mast cells reducing further mediator release.
Speaker 1:It tackles multiple problems at once.
Speaker 2:Exactly. The benefits in anaphylaxis vastly outweigh the potential risks which are actually quite low with a correct intramuscular dose. Delaying treatment allows the cascade to progress, making it harder to reverse.
Speaker 1:Okay, so the dose.
Speaker 2:For adults, the standard intramuscular dose is zero point three to zero point five milligrams. That's zero point three to zero point five milligrams of the one point one thousand concentration. Pediatric dosing is weight based. Zero point zero one milligrams per kilogram, typically up to a max of zero point three or zero point five milligrams depending on the guideline and patient size. Many use standard prefilled auto injector doses.
Speaker 2:Zero point one five milligrams for smaller children, zero point three milligram for larger children and adults.
Speaker 1:And route, you emphasized intramuscular.
Speaker 2:Yes, I'm is preferred. Studies show it provides faster absorption and higher peak plasma concentrations compared to subcutaneous injection. The vastus lateralis muscle, good blood flow, easy access.
Speaker 1:Got it. How often can we repeat the dose?
Speaker 2:You can repeat the I'm dose every five to ten minutes if the patient isn't improving or symptoms are progressing. Many patients only need one dose, but don't hesitate to give more if needed.
Speaker 1:And if they need multiple doses?
Speaker 2:If someone requires say two or three I'm doses and still isn't responding adequately, that's when you should strongly consider starting a continuous intravenous epinephrine infusion usually in an ICU setting with close monitoring.
Speaker 1:Okay. Any special considerations? Like patients on beta blockers?
Speaker 2:Yes, that's important. Patients on beta blockers can have a more severe or refractory reaction. Why? Because the beta blocker can blunt the effect of epinephrine on the beta receptors.
Speaker 1:Which are needed for bronchodilation and cardiac effects.
Speaker 2:Exactly, and it can leave the alpha adrenergic effects of epinephrine unopposed, potentially causing paradoxical hypertension or coronary vasoconstriction. So monitor BP very closely in these patients. They might need higher doses of epinephrine or sometimes glucagon.
Speaker 1:Glucagon, how does that help?
Speaker 2:Glucagon can increase intracellular KMP through a pathway independent of beta receptors potentially helping with heart rate and contractility when epinephrine isn't working well due to beta blockade but it has side effects like nausea and vomiting.
Speaker 1:Dr: Okay good to know so epinephrine is key What about fluids? You mentioned distributive shock?
Speaker 2:Right, anaphylaxis causes massive vasodilation and capillary leak, so patients become relatively volume depleted. Intravenous fluid resuscitation is crucial.
Speaker 1:What kind of fluids?
Speaker 2:Isotonic are the standard. Normal saline or lactated ringers. Give aggressive boluses often one-two liters for an adult or ten-twenty mmolg for kids. Repeat it as needed based on their response, blood pressure, and perfusion.
Speaker 1:Generally
Speaker 2:not indicated or shown to be superior to crystalloids in this setting. Stick with the basics.
Speaker 1:Okay, so epinephrine and fluids are the mainstays, what about all the other stuff we often give? Steroids, antihistamines, adjunctive therapies?
Speaker 2:Yes, those are the adjunctive therapies. They're often given but it's important to remember they are not first line treatments and should never delay epinephrine.
Speaker 1:Secondary measures.
Speaker 2:Exactly. They might help with refractory symptoms or theoretically prevent recurrence or biphasic reactions although the evidence for preventing biphasic reactions is debated.
Speaker 1:Let's talk steroids first. What's the rationale?
Speaker 2:Corticosteroids like methylprednisolone or hydrocortisone myV initially maybe oral prednisone are thought to reduce the length of the reaction and maybe that risk of a biphasic response by suppressing the later phase inflammation.
Speaker 1:Does the evidence strongly support that?
Speaker 2:The evidence specifically for preventing biphasic reactions in anaphylaxis is actually not very strong or consistent. But given their role in inflammation and other allergic conditions like asthma, they're still commonly used. Dosing often mirrors what we use for severe asthma.
Speaker 1:Okay. What about antihistamines H1 and H2 blockers?
Speaker 2:Antihistamines like diphenhydramine in H1 blocker are almost routinely given. They're primarily helpful for the skin symptoms, the itching and hives.
Speaker 1:Do they help with the life threatening parts?
Speaker 2:Their benefit for the really critical aspects like airway obstruction or hypotension in established anaphylaxis is considered minimal or unproven. Epinephrine is what saves lives, but they do help with cutaneous symptoms.
Speaker 1:And H2 blockers
Speaker 2:Adding an H2 blocker is sometimes done particularly for severe reactions or persistent skin symptoms. The theory is that blocking both H1 and H2 receptors might be more effective for some symptoms but again evidence is limited. Cimetidine has more interactions, so famotidine is generally preferred now.
Speaker 1:So helpful for skin, maybe some added effect, but not a replacement for epi?
Speaker 2:Absolutely not. Epi first, always. Antihistamines are supportive.
Speaker 1:Treatments like albuterol?
Speaker 2:Yes, inhaled bronchodilators typically beta agonists like albuterol sometimes combined with ipratropium are very useful if the patient has significant wheezing or bronchospasm.
Speaker 1:Especially if they have underlying asthma.
Speaker 2:Exactly. Patients with asthma are at higher risk for severe bronchospasm during anaphylaxis. If inhaled treatments aren't enough for refractory wheezing, IV Magnesium Sulfate can be considered, similar to how we use it in severe asthma exacerbations.
Speaker 1:Okay. And vasopressors, when would we use those?
Speaker 2:Vasopressors, other than epinephrine infusion, might be considered if the patient remains hypotensive despite adequate fluid resuscitation and multiple doses of epinephrine, or if they're having unacceptable side effects from high dose epinephrine, like severe arrhythmias.
Speaker 1:Is there a specific second line presser?
Speaker 2:There isn't clear consensus on a specific second line agent after epinephrine. You might consider norepinephrine or vasopressin, often guided by standard septic or distributive shock principles. But epinephrine really remains the primary vasopressor for anaphylactic shock.
Speaker 1:Got it. You mentioned glucagon for beta blocker patients. Any other specific adjuncts or research areas?
Speaker 2:Well, glucagon is the main one for refractory beta blocker associated anaphylaxis. Research wise, there's always ongoing work looking at the signaling pathways like that SER-two 16 idea, trying to find new ways to potentially modulate the mast cell response in the future. But clinically right now it's Epi, fluids, and the standard adjuncts.
Speaker 1:Okay that's a great rundown of treatment. Now when we see someone with shortness of breath, wheezing, maybe some flushing, what else could be going on? What's the differential
Speaker 2:That's crucial. The differential is broad because the symptoms can overlap with many other conditions.
Speaker 1:Like what?
Speaker 2:Well, obviously simple urticaria or angioedema without systemic features. Severe asthma exacerbation is a big one to differentiate.
Speaker 1:Oh, you tell them
Speaker 2:Anaphylaxis usually has multi system involvement in skin, GI, cardiovascular signs that you wouldn't typically see in isolated asthma, plus the trigger context. But it can be tricky if wheezing is the main feature. Anxiety or panic attacks can cause shortness of breath, palpitations, flushing. Vasovagal syncope causes hypotension and fainting but usually with bradycardia and pallor often after a specific trigger like pain or emotion not typically with hives or wheezing. Right.
Speaker 2:Cardiac issues like arrhythmias or even MI as we discussed with Cooney syndrome. Pulmonary embolism can cause sudden shortness of breath and hypotension. Then things like carcinoid syndrome which causes flushing and diarrhea due to tumor secretions, mastocytosis, a disorder of mast cells, even airway issues like epiglottitis or a foreign body obstruction or simple gastroenteritis if GI symptoms predominate. Vocal cord dysfunction can mimic wheezing or stridor.
Speaker 1:So a lot to consider. The key seems to be rapid onset multi system involvement and the context exposure.
Speaker 2:Exactly. History and the full clinical picture are key to narrowing it down quickly.
Speaker 1:Okay, so assuming we get the diagnosis right treat it quickly. What's the typical prognosis?
Speaker 2:Generally, with rapid recognition, appropriate treatment, especially epinephrine, and adequate monitoring, the prognosis is excellent. Most patients recover fully without lasting effects. Morbidity and mortality are low if it's managed properly. The danger lies in delayed treatment or misdiagnosis.
Speaker 1:Right, that first hour again?
Speaker 2:Doctor. Yes. Interestingly, despite how serious it is, only a relatively small percentage of all acute allergic reactions seen in the ED maybe less than four percent, actually require hospital admission.
Speaker 1:So most can go home after observation?
Speaker 2:If they respond fully to treatment, particularly if they needed epinephrine, meaning it was true anaphylaxis, and they remain stable during an observation period, yes.
Speaker 1:How long should we observe them?
Speaker 2:The general recommendation is typically around four to six hours minimum, specifically to watch for that biphasic reaction. They remain completely symptom free, didn't require multiple interventions, and have good follow-up arranged, they can often be discharged.
Speaker 1:Who needs admission?
Speaker 2:Definitely anyone who required airway intervention, had refractory symptoms needing prolonged treatment like an Epidrip, or remains unstable, they'd usually go to an ICU setting.
Speaker 1:What about longer observation or admission for less severe cases?
Speaker 2:You might consider longer observation or admission for patients with a history of very severe or biphasic reactions in the past. Those taking beta blockers, older patients, those who live alone or have poor access to care, or anyone who just feels at higher risk for recurrence or complications.
Speaker 1:Makes sense. And for discharge, what prescriptions and instructions are vital?
Speaker 2:This is critical for preventing future severe episodes. They absolutely need a prescription for an epinephrine auto injector. Often two are prescribed so they can keep one at home, one at work or school, or carry one.
Speaker 1:And instructions on how to use it.
Speaker 2:Thorough education is essential: how to recognize symptoms, when to use the auto injector, how to use it correctly, practice with a trainer device if possible, and the importance of calling emergency services immediately after using it.
Speaker 1:Always call 911 even if they feel better.
Speaker 2:Yes, absolutely. They need evaluation after using epinephrine. Also, emphasize having twenty four hour access to it if symptoms recur.
Speaker 1:What else other prescriptions?
Speaker 2:Often they'll get prescriptions for antihistamines and a short course of corticosteroids maybe for three to five days. Some argue for a longer steroid taper if the trigger is unknown or follow-up is uncertain, though evidence is still debated. Crucial follow-up with an allergist or immunologist should be arranged to help identify triggers, confirm the diagnosis if needed, and develop a long term management and avoidance plan.
Speaker 1:Should they consider medical alert jewelry?
Speaker 2:Yes, recommending a medical alert bracelet or necklace identifying their allergy and risk of anaphylaxis is a very good idea.
Speaker 1:Anything else for specific patient groups, like those beta blocker patients?
Speaker 2:For patients on beta blockers who've had a severe reaction, it's worth discussing with their primary care doctor or cardiologist whether alternative medications for their underlying condition might be possible given the increased risk during anaphylaxis.
Speaker 1:Got it. Lastly, what are the main complications we worry about if things go wrong?
Speaker 2:The immediate life threatening complications are airway obstruction leading to hypoxemia, persistent hypotension leading to shock and end organ and ultimately cardiovascular collapse and death. Even with recovery severe hypoxia could potentially lead to anoxic brain injury. Which brings us back to the importance of rapid recognition and treatment.
Speaker 1:Well that was a truly comprehensive and I think incredibly helpful deep dive into anaphylaxis. Really useful.
Speaker 2:Glad we covered it, it's such a core topic.
Speaker 1:Yeah, we've really gone through everything from basic definition, the triggers, the complex pathophysiology, those critical recognition points in a busy ED, and of course the management really hammering home that need for early epinephrine.
Speaker 2:Hopefully it reinforces those key actions.
Speaker 1:I think so. Hopefully this has provided really valuable insights and reinforced your understanding of this critical emergency useful for exams, useful for practice.
Speaker 2:Yeah.
Speaker 1:So join us next time on Mitzmoo Emergency Podcast. We'll be delving into another important topic in emergency medicine. Until then, stay safe and keep learning.
