REBEL Cast

Background: Massive pulmonary embolism  defined as sustained hypotension (SBP <90mmHg)  has a high mortality which is why early recognition and thrombolytic therapy is typically recommended (AHA Class IIA; ESC Class IB) [1]. However, full-dose thrombolytic therapy (Alteplase 100mg (IV) is  associated with an increase in bleeding [2]. Because the lungs receive 100% of cardiac output, it has been hypothesized that a lower dose of thrombolytic therapy may still be effective with a better safety profile [3][4]. REBEL Cast Ep123:  Reduced-Dose Systemic Peripheral Alteplase in Massive PE? Click here for Direct Download of the Podcast Paper: Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358 Clinical Question: What is the efficacy and safety  of low-dose (25mg) prolonged administration (over 6hrs) of alteplase in patients with massive PE? What They Did: Single-center, pilot prospective observational cohort trial in Turkey Thrombolysis 25mg of alteplase without a bolus was administered over 6 hours by peripheral IV infusion If hemodynamic instability persisted despite first dose of thrombolysis, a second 6hr infusion of 25mg alteplase without bolus was administered (No patients in the study required this) Did not use concomitant heparin anticoagulation with thrombolysis Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed Patients were all converted to warfarin for discharge TTE All patients underwent TTE before thrombolysis, within an hour after thrombolysis, before discharge (5 to 7d) and a month after thrombolysis PASP estimated from tricuspid valve regurgitant jet velocity Maximum dimension of RA/LA measured in 4-chamber view Diameter and collapsibility of IVC noted Pulmonary HTN defined as PASP >40mmHg RV enlargement defined as RV/LV ratio >0.9 Tricuspid Annular Plane Systolic Excursion (TAPSE) also recorded Tissue Doppler Derived Tricuspid Annular Systolic Velocity recorded Tei-Myocardial Performance Index (MPI/Tei) recorded CT All patients underwent 64 slice CTPA for definitive diagnosis of PE at admission Additional CTPA 24 hours after completion of thrombolysis if eGFR >60mL/min/1.73m2 Criteria for Thrombolytic Success Included: Doppler documentation of resolution of increased PASP (<40mmHg) Decreased RV diameter (at least 25% decrease of RV/LV diameter) Restoration of RV function (TAPSE>16mm) Systolic Wave Prime (S’) >10.0cm/s Tissue Doppler Derived RV MPI > 0.55 Clinical improvement of symptoms and restoration of stable hemodynamic status immediately after thrombolysis Complete success = Clinical improvement of symptoms and restoration of a stable hemodynamic status along with at least 3 other criteria without resultant death and nonfatal major complications Outcomes: Primary: In-hospital mortality Major complications Ischemic stroke, ICH, embolism (coronary or peripheral), bleeding requiring transfusion Pulmonary HTN while in hospital RV dysfunction while in hospital Secondary: 6 month mortality Development of pulmonary hypertension at 6 months RV dysfunction at 6 months Inclusion: Adult patients (≥18 years of age) Confirmed massive PE Massive PE Definition Acute PE with sustained hypotension (SBP <90mmHg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LV dysfunction) Pulselessness Persistent profound bradycardia (HR<40BPM with signs or symptoms of shock) Exclusion: Prior ICH Known structural intracranial cerebrovascular disease (i.e. AV malformation) Known malignant intracranial neoplasm Ischemic stroke within 3 months Suspected aortic dissection Active bleeding or bleeding diathesis Recent surgery encroaching on the spinal canal or brain Recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury Results: 37 consecutive patients with massive PE were enrolled Blood pressure recovered within a few hours after initiation of thrombolysis in all cases Mortality Primary Efficacy Outcome: 1 in-hospital death (3.1% in the paper but 2.7% in table 2) on day 6 of hospitalization due to malignant ventricular arrhythmia (Pt had ischemic dilated cardiomyopathy with LVEF of 20% and acute on chronic renal failure) 2 additional deaths within 6 months (Both pts had malignancy) Not implicitly stated whether these deaths are attributed to PE, however it doesn’t sound like they are based on the patient descriptions TTE Results from Admission to Post Thrombolysis: Primary Efficacy Outcome: Mean PASP ≈57mmHg to 34mmHg (p<0.001) Mean PASP continued to decrease prior to discharge ≈34mmHg to ≈30mmHg (p<0.001) Mean PASP preserved at 6 month follow up ≈29mmHg No patients with pulmonary hypertension at 6 months Primary Efficacy Outcome: Mean TAPSE ≈1.43cm to 2.07cm (p<0.001) RV/LV Diameter ≈1.37 to ≈0.99 (p<0.001) Mean MPI/Tei Index≈ 0.47 to ≈0.55 (p<0.001) Systolic Wave Prime (S’) ≈10 to ≈15 Follow Up CTPA 24hrs After Thrombolysis Out of 37 patients, 18 (56.3%) underwent repeat CTPA 24hrs after thrombolysis Out of these 18 pts total lysis of thrombus was observed in 16pts (88.9%) and the remaining 2pts had >75% lysis of thrombus Complications Post Thrombolysis: Primary Safety Outcome: No major bleeding or stroke observed 3 patients with minor bleeding 2pts with epistaxis (2 days after thrombolysis) 1pt with gingival bleeding (3 days after thrombolysis) All bleeding events occurred during heparin infusion and stopped with gentle compression without recurrence 6pts (17.6%) had major bleeding and 2pts (5.68%) had minor bleeding due to warfarin Strengths: Consecutive patients enrolled which minimizes selection bias All patients followed for 6 months (No loss to follow up) Limitations: Single center, nonrandomized observational trial No comparison group receiving standard therapy (i.e. compared to half-dose 50mg or full dose 100mg of alteplase) Small sample size with few complications makes this an underpowered study to make any firm conclusions about bleeding risks Lots of missing methodology Unclear what time period patients were recruited How strict were authors in consecutive recruitment (? selection bias) Unclear therapies prior to lytics (i.e. Pressors, heparin, etc) Who performed echos and unclear degree of consistency (Echo has some subjectivity to it) Discussion: PE is a Spectrum of Disease Massive PE is also a spectrum of disease This study doesn’t appear to include critically ill massive PE patients who are peri-arrest Dripping alteplase over 6 hours is most likely not going to be the appropriate therapy in the more severe massive PE patients Primary Efficacy Outcome Multiple primary efficacy outcomes were listed in this study, which can be problematic when you get multiple outcomes of varying statistical significance. In this trial all the primary efficacy outcomes were statistically significant, and the authors clearly defined what they meant by complete success in this trial Complications While in Hospital No cases of major bleeding or ICH in this study The 3 patients who had minor bleeding at 48 to 72hrs were most likely due to the heparin infusion and not associated with thrombolysis The cohort is simply too small with not enough complications for the study to be powered correctly for this outcome IV Access These authors gave alteplase through a peripheral IV which we do in stroke patients, but that is typically done over 1hr not over 6hrs If I was going to do this (25mg alteplase over 6hrs) I would want a central venous catheter to avoid the potential of infiltration or if the patient decompensates further and needs central venous access after the fact there is a higher risk of hematoma/bleeding Also, I would already have an arterial line in place before starting thrombolysis for continuous hemodynamic monitoring Heparin Dosing Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed Prior studies have found marked increase in bleeding when lytics and heparin are given together After thrombolysis I typically don’t bolus heparin and just start the infusion Also I don’t start the heparin infusion immediately after thrombolysis, I wait for the PTT to be <2x the control before starting A dose of 0.5 to 4.0mg/hr typically given in EKOS therapy (See Below). This trial gave 25mg over 6hrs (≈4mg/hr) ULTIMA Trial [5]: 59pts with massive/submassive PE Used alteplase at a dose of 1mg/hr x5hrs, then 0.5mg/hr x10hrs Max Dose ≈20mg No major bleeding SEATTLE II Trial [6]: 150pts with massive/submassive PE Used alteplase at a dose of 1mg/hr x24hrs Max Dose ≈25mg 1 severe/life-threatening hemorrhage (Groin hematoma requiring vasopressor support) No ICH OPTALYSE-PE Trial [7]: 101pts with submassive PE Used alteplase at a dose of 8mg/2hrs (4mg/hr), 8mg/4hrs (2mg/hr), 12mg/6hrs (2mg/hr), and 24mg/6hrs (4mg/hr) Max Dose 24mg No major bleeding with 8mg/2hrs, 8mg/4hrs, and 12mg/6hrs 2 major bleeding episodes occurred in the 24mg/6hr group The max dose any patients got was ≈25mg (Max Dose Range ≈20mg to ≈25mg). Major bleeding seemed to occur in the drips that ran for over 15hrs (3 pts out of 310 [≈1%]); But no cases of major bleeding for drips ≤15hrs To take this one step further this trial raises the question of whether EKOS even necessary or is it an overly expensive intervention that potentially increases complications without improving outcomes? Although this was not a randomized clinical trial and there was no comparator arm we do have two trials on submassive PE with half-dose alteplase (50mg) given over 2hours [8] and half-dose alteplase (50mg) given in Massive PE [3] MOPETT Trial [8] 121pts with submassive PE (Called “moderate PE” in the study) Randomized to half dose thrombolysis vs anticoagulation alone For patients weighing ≥50kg a total dose of 50mg given (10mg bolus by IV push followed by 40mg infusion over 2hrs) For patients weighing <50kg a total dose of 0.5mg/kg given (10mg bolus by IV push followed by the remainder over 2hrs) Primary endpoints consisted of pulmonary HTN and composite of pulmonary HTN and recurrent PE at 28mos Pulmonary HTN at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone Composite Pulmonary HTN and Recurrent PE at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone There were 0 cases of bleeding in either arm PEAPETT Trial [3] 23 patients with PEA cardiac arrest due to confirmed massive PE All pts received 50mg of alteplase as an IV push while CPR was ongoing ROSC occurred in 2 to 15 min after alteplase administration in all but one patient There was no minor or major bleeding despite chest compressions What this current trial [9] is really adding to the literature is an even lower dose of thrombolysis (25mg) efficacious? We already know from the MOPETT trial [8] and PEAPETT trial [3] that half-dose alteplase (50mg) had zero cases of bleeding so this current trial just tells us what we already know. 25mg of alteplase has less risk of bleeding than 50mg of alteplase Additionally, if 25mg can treat massive PEs [9], this could also be extrapolated to less severe high-risk submassive PEs (Although I would still love to see a head-to-head trial of 25mg vs 50mg) Author Conclusion: “Results of this pilot study suggest that low-dose prolonged infusion of tPA is an effective and safe therapy in patients with massive PE. This protocol was also effective in decreasing PASP and restoration of RV function.”  Clinical Take Home Point: Low dose (25mg) alteplase given as a prolonged infusion (over 6hrs) is a promising effective and safe therapy in patients with massive PE and provides an alternative to full dose (100mg) and half-dose (50mg) alteplase. Larger RCTs comparing doses of alteplase are warranted to confirm these findings. References: Jaff MR et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement from the American Heart Association. Circ 2011. PMID: 21422387 Wan S et al. Thrombolysis Compared with Heparin for the Initial Treatment of Pulmonary Embolism: A Meta-Analysis of the Randomized Controlled Trials. Circ 2004. PMID: 15262836 Sharifi M et al. Pulseless Electrical Activity in Pulmonary Embolism Treated with Thrombolysis (from the “PEAPETT” Study). AJEM 2016. PMID: 27422214 Wang C et al. Efficacy and Safety of Low Dose Recombinant Tissue-Type Plasminogen Activator for the Treatment of Acute Pulmonary Thromboemolism: A Randomized, Multicenter Controlled Trial. CHEST 2010. PMID: 19741062 Kucher N et al. Randomized, Controlled Trial of Ultrasound-Assisted Catheter-Directed Thrombolysis for Acute Intermediate-Risk Pulmonary Embolism. Circ 2014. PMID: 24226805 Piazza G et al. A prospective, Single-Arm Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACCC Cardiovasc Interv 2015. PMID: 26315743 Tapson VF et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Reisk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc Interv 2018. PMID: 30025734 Sharifi M et al. Moderate Pulmonary Embolism Treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013. PMID: 23102885 Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358 For More Thoughts on This Topic Checkout: EMCrit: EMCrit 354 – Reduced-Dose Systemic Peripheral Fibrinolysis in Massive Pulmonary Embolism Post Peer Reviewed By: Anand Swaminathan, MD (X: @EMSwami) The post REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE? appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Achilles tendon rupture is a clinical diagnosis. The Thompson Test should be applied in all suspected cases. Remember to brace or splint a rupture, even if suspected, in the resting equinus position for optimal healing and prevention of further injury. Schedule follow up with orthopedics within 1 week for discussion of operative management vs early rehab protocols. REBEL Core Cast 116.0 – Achilles Tendon Rupture Click here for Direct Download of the Podcast Achilles Tendon Rupture Exam (www.lfaclinic.co.uk) Physical Exam May have palpable gap or deformity in region of tendon. Weakness with plantar flexion. Increased resting ankle dorsiflexion on affected side in prone position with knees bent . Usually in absence of bony tenderness unless accompanied by other injury Thompson Test (video) Place the patient in the prone position, with feet hanging over the end of a stretcher or table. If patient is not able to lay down/there are no stretchers, the patient can kneel on a stool or chair Squeeze the calf of the normal limb. You will notice the squeeze will cause the ankle to plantarflex appropriately Squeeze the calf of the limb with the suspected Achilles tendon rupture.  You will notice the squeeze will cause no motion if there is a full rupture/tear, and diminished motion if there is a partial tear Performance Characteristics (Garras 2012) Sensitivity Specificity (+) LR (-) LR 96-100% 93-100% 13.7 0.04 Imaging X-Rays Used to rule out other or concurrent pathology May show soft tissue swelling and destruction of pre-Achilles fat pad (Kager’s Fat Pad) Findings are non-specific as tear of tendon unable to be visualized Ultrasound Ultrasound is helpful if obvious findings present and to distinguish between partial vs complete tears, however only around 50% sensitive for detecting only partial tears (Kayser 2005) MRI Gold-standard imaging modality Rarely, if ever, necessary in the ED Used for equivocal physical exam/alternate imaging findings or for assessing the severity of the tear for possible operative management Findings A full-thickness tear often shows a tendinous gap filled with edema or blood Complete rupture shows retraction of tendon ends ED Management Provide analgesia Tendon stabilization in an optimal healing position Functional bracing/splinting in resting equinus/talipus equinus AO splint/brace in 20 degrees of plantar flexion for 4-6 weeks (may use tall CAM boot with 20 degrees wedge inserts) All patients should be non-weightbearing Any weight-bearing can convert a partial tear to a complete tear Maintain non-weightbearing status until see orthopedics (within 1 week) After evaluation by orthopedics, early weight-bearing and early ROM exercises yield better outcomes (can be as early as 2 weeks) Referral to rehab warranted to improve plantar flexion and decrease risk of re-rupture ED Ortho consultation: patients with open wounds in the area of trauma, or with concomitant fractures Operative Management is usually reserved for acute ruptures (approximately <6 weeks) of full thickness with large tendon gaps, failed conservative treatment of partial thickness tears, or high performance athletes These cases will be determined during follow up with orthopedics and may warrant outpatient MRI to assess severity of tear Prognosis For conservative management, there is no significant difference in plantar flexion strength (Willits, 2010) Some increased risk of re-rupture compared to operative management, although review of evidence shows that this may not be significant if patients used structured, accelerated rehab protocol. Protocol includes initially non-weightbearing cast with the foot in equinus position as described above, then transitioned to a pneumatic walker with elevated heels (elevation gradually reduced biweekly), and physical therapy to improve gait, strength, and mobility. (Wallace 2011) If addressed early and appropriately, most patients have good self-reported long-term outcomes regardless of the treatment modality Links Orthobullets: Achilles Tendon Rupture Resources: Sheth U et al. The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27,607 patients. Bone Joint J. 2017; 99-B(1): 78-86. PMID: 28053261 Chiodo CP, Wilson MG. Current Concepts Review: Acute Ruptures of the Achilles Tendon. Foot Ankle Int 2006; 27(4): 305-13. PMID: 16624224 Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med. 1998; 25(2): 79-100. PMID: 9519398  Kayser R et al. Partial rupture of the proximal Achilles tendon: a differential diagnostic problem in ultrasound imaging. Br J Sports Med. 2005; 39(11): 838-42. PMID: 16244194 Margetic P et al. Comparison of ultrasonographic and intraoperative findings in Achilles tendon rupture. Coll Antropol. 2007; 31:279-284. PMID: 17598414 Garras DN et al.  MRI is Unnecessary for Diagnosing Acute Achilles Tendon Ruptures: Clinical Diagnostic Criteria. Clin Orthop Relat Res 2012; 470(8): 2268-2273. PMID: 22538958 Willits K et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial using accelerated functional rehabilitation .J Bone Joint Surg Am. 2010; 92(17): 2767-75. PMID: 21037028 Wallace RG et al. The non-operative functional management of patients with a rupture of the tendo Achillis leads to low rates of re-rupture. J Bone Joint Surg Br 2011; 93(10):1362-6. PMID: 21969435 Erickson BJ. Is Operative Treatment of Achilles Tendon Ruptures Superior to Nonoperative Treatment? Orthop J Sports Med. 2015; 3(4): PMID: 26665055 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 116.0 – Achilles Tendon Rupture appeared first on REBEL EM - Emergency Medicine Blog.

In this episode, Martin Amour, a critical care cardiologist and director of the CCU at Staten Island University Hospital, shares insights on managing cardiogenic shock. He discusses key clinical signs like cold extremities and confusion, and highlights the importance of early lactate measurement as a danger sign. Amour explains the effective use of norepinephrine as a first-line treatment and dobutiline for inotropic support. He also delves into innovative devices like impella CP and ECMO, focusing on personalized approaches for young patients and the urgency of interdepartmental collaboration.

Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes. Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin. Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities). REBEL Core Cast 114.0 – Carbon Monoxide Toxicity Click here for Direct Download of the Podcast Definition and Physiology Carbon monoxide is absorbed via inhalation from the incomplete combustion of any carbon containing substance. Most often, exposures often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. Toxicity is mediated through multiple mechanisms. Physiologic oxygen carrying capacity is reduced as carbon monoxide binds hemoglobin with a greater affinity than oxygen. Moreover, carbon monoxide shifts the oxygen-hemoglobin dissociation curve to the left which reduces oxygen delivery to tissues. Lastly, carbon monoxide effects cellular oxygen use by impairing oxidative phosphorylation by binding to mitochondrial cytochromes. (Goldbaum 1976) Clinical Manifestations Acute, mild toxicity presents non-specifically. Given that most exposures will occur during the winter months, a common misdiagnosis is influenza or the “common cold.” Symptoms include: headache, dizziness, nausea, vomiting, and generalized weakness. More severe toxicity will present with syncope, altered mental status, neurologic disturbance (ie. ataxia), myocardial ischemia, or cardiac arrest. Carbon monoxide poisoning may lead to delayed neurologic sequalae – a constellation of dementia, psychosis, parkinsonism, amnestic syndromes, among other neurologic impairments. Management Carbon monoxide testing is performed via co-oximetry which determines the amount of carboxyhemoglobin present. The mainstay of treatment is supplemental oxygenation. The half-life of carboxyhemoglobin drops from 5 hours on room air to 1 hour when breathing 100% oxygen at normal atmospheric pressure (via non-rebreather). Hyperbaric treatment should be considered for severe toxicity. (Goldfrank’s Toxicology 2019) Carboxyhemoglobin levels > 25% or >15% in pregnant patients are indications for hyperbarics, independent of signs/symptoms There is evidence that hyperbaric oxygenation reduces the risk of cognitive sequelae after acute carbon monoxide poisoning. (Weaver 2002) As always, call your local toxicologist or regional poison control center to help determine the need for hyperbaric therapy.   Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes. Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin. Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities). References Goldbaum LR, Orellano T, Dergal E. Mechanism of the toxic action of carbon monoxide. Ann Clin Lab Sci. 1976 Jul-Aug;6(4):372-6. PMID: 962299. Tomaszewski C. Chapter 122. Carbon Monoxide. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed November 6, 2023. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1057-67. doi: 10.1056/NEJMoa013121. PMID: 12362006. Post Created By: Sanjay Mohan MD Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 114.0 – Carbon Monoxide Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points: All STEMIs should be loaded with dual antiplatelet therapy. Prasugrel (Effient) is avoided as there is an increase in bleeding complications if the patient requires a CABG. NSTEMI cases can be challenging to manage. Consult Cardiology early and use all available data. The appropriate medical treatment for ACS patients is as important as PCI. POCUS is a very valuable tool for ACS patients in the ED. Clinical presentation  trumps all other data. Trust your gut! REBEL Core Cast 113.0 – ACS Therapies and Management Click here for Direct Download of the Podcast Links Staten Island EM: Only in Staten Podcast Post Created By: Anand Swaminathan MD, MPH Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 113.0 – ACS Therapies and Management appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points: Dose your RSI meds correctly.  Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.   Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!  REBEL Core Cast 112.0 – Awareness During Paralysis Click here for Direct Download of the Podcast Awareness during paralysis is real. However, data is limited in ED patients. The ED AWARENESS study found a 2.6% rate of prevalence: meaning about  three in every one hundred people may experience awareness during paralysis.  We know that rocuronium has a longer half life than its counterpart succinylcholine. However, this is not the problem! The key is starting post-intubation sedation ASAP.  We need to keep this phenomenon in the back of our minds every time we intubate. Here are some things we can do to prevent awareness during paralysis:  Dose your RSI meds correctly.  Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.   Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!  References Pappal, Ryan D., et al. “The ED-AWARENESS study: A prospective, observational cohort study of awareness with paralysis in mechanically ventilated patients admitted from the emergency department.” Annals of emergency medicine 77.5 (2021): 532-544. Links Staten Island EM: Only in Staten Podcast Post Created By: Anand Swaminathan MD, MPH Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 112.0 – Awareness During Paralysis appeared first on REBEL EM - Emergency Medicine Blog.

Explore the benefits and limitations of coronary CTN geography as a cardiac test for low-risk chest pain patients. Learn about the importance of selecting appropriate tests based on symptoms and considering limitations. Understand the usefulness of CCTA and nuclear stress tests in assessing heart conditions. Trust your intuition alongside test results.

Take Home Points: Patients with recent onset atrial fibrillation can safely be cardioverted if they are 1) on anticoagulation 2) Low risk based on CHADS-VASC with onset < 48 hours or 3) High risk based on CHADS-VASC with onset < 12 hours. In anaphylaxis, think, “If A, B or C, give E.” If the patient has compromise to airway, breathing or circulation, they should get immediate epinephrine. D-dimer can effectively rule out a larger portion of low risk patients if age adjustment or the YEARS criteria are employed. When reviewing a syncope ECG, scour it for WPW, Brugada, Hypertrophic Cardiomyopathy, Prolonged/Short QTc and ARVC. REBEL Core Cast 110.0 – On Shift Learning Pearls Click here for Direct Download of the Podcast Links EM: RAP: Atrial Fibrillation Update REBEL EM: The Pragmatic Combination of YEARS Score and Age-Adjusted D-Dimer Core EM: Age-Adjusted D-dimer (Using DDU) REBEL EM: Anaphylactic Shock REBEL EM: Core Cast 21.0 – ECG in Syncope Post Created By: Anand Swaminathan MD, MPH Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 110.0 – On Shift Learning Pearls appeared first on REBEL EM - Emergency Medicine Blog.

This podcast discusses the significance of ECG in evaluating overdose patients and the connection between QRS prolongation and sodium channel blockade. It explores ECG changes seen in tricyclic antidepressant and Diphenhydramine overdoses. The importance of considering sodium channel blockade as a differential diagnosis for widened QRS intervals is highlighted. Treatment recommendations for wide, complex tachycardia caused by sodium channel blockade with sodium bicarbonate are provided.

Take Home Points: Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise. Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management. Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction. REBEL Core Cast 108.0 – Angioedema Click here for Direct Download of the Podcast Angioedema: A transient, localized, non-pitting distention of the skin (subcutaneous layer) or the respiratory and gastrointestinal tracts (submucosal layer) Inflammatory mediators cause vascular permeability, allowing fluid to diffuse into the interstitium    Effects areas with loose connective tissue, like the oropharynx, extremities, and genitalia Epidemiology: 0.1 to 0.3% of people who take NSAIDs (Nzeako 2010). 0.1 to 0.7% patients that take ACE inhibitors (but 20-30% of all angioedema presentations to the Emergency Department) 3 times more common in Black Americans (Kostis 2005) 0.01 to 0.002% of general population exhibit some form of hereditary angioedema (Zuraw 2008) Mechanism and Pathophysiology: Mast Cell Mediated Bradykinin Mediated Other IgE Dependent ACE-Inhibitor Infectious IgE Independent Hereditary Angioedema Iatrogenic NSAIDs Acquired C1 Inhibitor Deficiency Idiopathic Mast Cell (granulocyte) Mediated Mast cell activation (by IgE crosslinking or directly) leads to the generation of mediators (histamine, heparin, leukotriene and prostaglandin D2), which increases vascular permeability. Features Urticaria and pruritis Rapid onset (1-2 hours) IgE Dependent (Type I Hypersensitivity) Reactions An allergen cross-links two or more IgE molecules on mast cells or basophils and initiates a signal cascade leading to degranulation. Pro-inflammatory mediators then act on the mucosa and cause angioedema. These chemicals can recruit other cells, like eosinophils, and may lead to anaphylaxis. IgE Independent Reactions Mast cells are activated directly by certain medications (i.e. meperedine, radiocontrast agents) Release inflammatory mediators and lead to angioedema. NSAIDs hinder the formation of prostaglandins within mast cells and other leukocytes. This can cause an abundance of leukotrienes and other pro-inflammatory mediators and precipitate angioedema (Nzeako 2010). Bradykinin Mediated Plasma globulins called kininogens release bradykinin and cause vascular permeability. Features Absence of urticaria and pruritus Insidious onset (24-36 hours) ACE Inhibitors Inhibition of ACE hinders the degradation of bradykinin and can lead to idiosyncratic angioedema. Typically involves the mouth, larynx, pharynx, and subglottic tissue (Kostis 2005). Hereditary Angioedema (presents in childhood) and Acquired C1 Inhibitor Deficiency (adulthood) Both involve abnormalities in the level or function of the C1 inhibitor. Without the C1 inhibitor, the plasma-kallikrein-kinin system produces more bradykinin. Both conditions can range in severity from benign to life threatening (Wilkerson 2012). Other Etiologies In pediatrics, illnesses like the common cold, Streptococcus pyogenes (GAS) pharyngitis, and urinary tract infections can cause isolated angioedema (without urticaria). Iatrogenic agents like calcium channel blockers, fibrinolytic agents, estrogens, and herbal supplements Idiopathic Differential: Anaphylaxis Erysipelas or cellulitis Contact dermatitis Superior vena cava syndrome Hypothyroidism Peritonsillar abscess Autoimmune disease Parasitic Infection Presentation: Asymmetrical Does not regularly involve gravitationally dependent areas Frequently painless Non blistering, non desquamating Hives, pruritus, bronchospasm or flushing = mast cell release (histaminergic) Abdominal pain, nausea, vomiting Hoarse voice Stridor Drooling, difficulty swallowing Throat tightness Inability to phonate high pitched “E” sound Management: Basics- ABCs, IV, O2, Cardiac Monitor Anatomically challenging airway Edema of the anterior tongue, base of the tongue, or larynx significantly increases the likelihood of intubation or tracheostomy. Stable patients with isolated anterior tongue edema should undergo fiberoptic laryngoscopy in the ED (McCormick 2011) Avoid unnecessary airway manipulation (can exacerbate edema) Edema may obscure the neck anatomy Airway Management Early intubation often indicated as swelling may progress and supraglottic rescue devices may be ineffective Consider awake intubation Double setup with standard intubation equipment and surgical airway tools for possible failed orotracheal airway Can’t intubate, cant ventilate event necessitates surgical airway Do not rely on external anatomy for cricothyroidotomy as edema will obscure landmarks (Hessert 2013) Plan for a large vertical incision in the midline of the neck Directed Treatment Mast cell mediated (histaminergic) angioedema Epinephrine 300 to 500 mcg IM H1 antihistamines Diphenhydramine 25-50 mg PO/IM/IV Cetirizine 5-10 mg PO H2 antihistamines Ranitidine 50 – 150 mg PO/IV Glucocorticoids: Methylprednisolone 1-2mg/kg per day x 2 days Bradykinin mediated angioedema Unlikely to respond to epinephrine, antihistamines, or glucocorticoids Hereditary Angioedema and C1 esterase deficiencies (Wilkerson 2012) Replace C1 inhibitor with Berinert 20units/kg IV (harvested from pooled human plasma) Antagonize kallikrein with Ecallantide 30mg IM Antagonize bradykinin b2 receptor with Icatibant 30mg SQ Replace ACE with 2 units FFP (2nd line) ACE inhibitor related angioedema Discontinue ACE Inhibitor Secure airway, supportive care Icatibant A single randomized controlled trial comparing Icatibant with prednisone and antihistamines demonstrated more rapid improvement of symptoms with Icatibant (Bas 2015) CAMEO: phase III, double blind, placebo controlled trial showed no benefit. Fresh Frozen Plasma (FFP) Case reports and case series have shown a benefit from FFP (Wilkerson 2012, Hassen 2013) However, FFP also contains bradykinin and high molecular weight kininogen which may exacerbate angioedema Tranexamic Acid (TXA) TXA inhibits the conversion of plasminogen to plasmin which, in theory, could reduce bradykinin production. Low quality evidence (case reports and case series) have hinted at benefit but are mixed. There is no high-quality evidence to support its use and no safety data. Take Home Points: Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise. Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management. Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction. Read More EMCrit: Podcast 145 – Awake Intubation Lecture from SMACC ERCast: Angioedema References: Baş M et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema.  N Engl J Med. 2015; 372(5):418-25. PMID 25629740 Hassen GW et al. Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema. J Emerg Med 2013; 44 (4): 764-772. PMID: 23114109 Hessert MJ and Bennett BL. Optimizing Emergent Surgical Cricothyrotomy for Austere Environments. Wilderness and Environmental Medicine. 2013;24:53-66. PMID 23062323 Kostis JB et al. Incidence and characteristics of angioedema associated with enalapril. Arch Intern Med. 2005;165(14):1637-1642. PMID 16043683 McCormick M et al. Site involvement as a predictor of airway intervention in angioedema. Laryngoscope. 2011;121:262–266. PMID 21271571 Morgan PB. Hereditary angioedema—therapies old and new. N Engl J Med. 2010;363(27):2673. PMID 20818894 Nzeako UC. Diagnosis and management of angioedema with abdominal involvement: A gastroenterology perspective. World J Gastroenterol, 2010;16(39):4913-4921. PMID 20954277 Sinnert R et al. Randomized Trial of Icatibant for Angiotensin- Converting Enzyme InhibitoreInduced Upper Airway Angioedema (CAMEO Study). J Allergy Clin Immune Tract 2017; 5(5): 1402-9. PMID: 28552382 Wilkerson RG. Angioedema in the Emergency Department: An Evidence Based Review.  Emergency Medicine Practice. EBMedicine.net. 2012; 14(11). Zuraw et al. An overview of angioedema: Clinical features, diagnosis, and management. In: UptoDate, Feldweg AM (ed.) UpToDate, Waltham, MA. Zuraw BL. Clinical practice. Hereditary angioedema. N Engl J Med. 2008;359(10):1027-1036. PMID 18768946 Post Created By: Anand Swaminathan MD, MPH (Twitter @EMSwami) Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie) The post REBEL Core Cast 108.0 – Angioedema appeared first on REBEL EM - Emergency Medicine Blog.