REBEL Cast

Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. The key is in identifying and rapidly gaining control with a posterior pack or foley catheter. These patients often require surgical intervention so get ENT to the bedside and admit to a place with a higher level of monitoring. REBEL Core Cast 123.0 – Posterior Epistaxis Click here for Direct Download of the Podcast. Recognition Typically will have heavy bleeding both anteriorly and posterior into the oropharynx. These patients have a tough time because they’re continually trying to spit out or swallow blood Tachycardia is common and hypotension while not common isn’t unexpected. Very different from anterior epistaxis where VS usually unremarkable or maybe a bit of hypertension Failure of anterior pressure or packing to stop bleeding: apply pressure but still see brisk posterior bleeding or even place b/l pack and see continued posterior bleeding Start with the basics IV, Supp O2, Monitor Consider blood products if the patient appears to be losing a lot of blood or they report heavy blood loss. VS abnormalities can drive this as well Strongly consider reversal of AC (this will typically come after control) Stopping the Bleeding PPE: these things bleed like stink. Anecdote. Gown, gloves and most importantly eye and face protection Ideal: commercial posterior pack Two balloons – one for anterior, one for posterior Place the device (straight back parallel to the floor) Inflate anterior balloon (10-15 cc) of air If still bleeding, inflate posterior balloon (5-10 cc of air) Foley: if no commercial device Place foley catheter just as you would place a nasal tampon When you see the tip of the foley in the posterior pharynx, inflate balloon (5-10 cc) Need to pull back a bit and secure (can do this with tape on the nose) Post Placement Care Antibiotics: standard practice to give cephalexin or amox/clav. Literature doesn’t defend this approach but, the lit is pretty sparse. The idea behind abx is to prevent things like AOM and TSS but neither should be much of an issue with short term placement ICU Admission? Traditional teaching is that these patients are at risk for life-threatening bradydysrhythmias and should go to the ICU Literature here is non-existent. Two oft-cited articles Cassisi Laryngoscope 1971 – no mention of cardiac events in the article but widely cited Zeyyan Laryngoscope 2010 – slightly lower HR in the packing group but no bradydysrhythmias Before throwing ICU out Hypoxia can occur – Cassisi found about a 20 mm Hg drop in PaO2 but all the patients in this publication were sedated so the packing may not have been the issue look at Viducich 1995 Acad Emerg Med – showed that 18% of the 88 patients with posterior epistaxis required a surgical intervention. With that in mind, you want to consider placing patients into a setting where they can be frequently reassessed – perhaps SDU. This will be pretty location specific. If you treat a posterior bleed at a hospital without ENT, I would transfer as surgical intervention is pretty common REBEL EM: Do Patients with Epistaxis Managed by Nasal Packing Require Prophylactic Antibiotics? REBEL EM: Do Patients with Posterior Epistaxis Managed by Posterior Packs Require ICU Admission? EMRAP HD: Epistaxis Posterior Pack References Cassisi NJ et al. Changes in arterial oxygen tension and pulmonary mechanics with the use of posterior packing in epistaxis: a preliminary report. Laryngoscope 1971; 81(8): 1261-6. PMID: 5569677 Zeyyan E et al. The effects on cardiac function and arterial blood gas of totally occluding nasal packs and nasal packs with airway. Laryngoscope 2010; 120: 2325-2330. PMID: 20938948 Loftus BC et al. Epistaxis, medical history and the nasopulmonary reflex: what is clinically relevant. Otolaryngol Head Neck Surg 1994; 110: 363-9. PMID: 8170679 Viducich RA et al. Posterior epistaxis: clinical features and acute complications. Acad Emerg Med 1995; 25(5): 592-6. PMID: 7741333 Corrales CE, Goode RL. Should patients with posterior nasal packing require ICU admission. Laryngoscope 2013; 123: 2928-9. PMID: 24114977 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 123.0 – Posterior Epistaxis appeared first on REBEL EM - Emergency Medicine Blog.

Background: In May of 2018, Andexanet alfa gained accelerated approval by the FDA for the reversal direct oral anticoagulants (DOACs) despite a lack of robust evidence for use. The 2022 AHA/ASA guidelines give the drug a level 2A recommendation and recommend it over the use of 4F-PCC (Greenberg 2022). FDA approval alongside guideline endorsement has led to the drug seeing a remarkable growth in use without a single high-quality study to support its use. The available data reports good hemostatic control: a subjective measure that is highly biased by unblinding and selection bias. More importantly, there are no studies comparing andexanet alfa to 4F-PCC or even placebo looking at important, patient-centered outcomes. REBEL Cast WEE – ANNEXA-1 – Andexanet Alfa Associated with Harm in DOAC Reversal Click here for Direct Download of the Podcast. Article: Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032 Clinical Question: Does the use of andexanet alfa in patients on DOACs with intracerebral hemorrhage improved hemostatic efficacy? Population: Patients > 18 years of age on a factor Xa inhibitor (taken within 15 hours of randomization) with an acute intracerebral hemorrhage. Outcomes: Primary: Hemostatic efficacy assessed at 12 hours after randomization. Hemostatic efficacy was defined as: Excellent hemostatic efficacy: Change in hematoma volume < 20% Good hemostatic efficacy: Change in hematoma volume < 35% Increase in NIHSS < 7 points at 12 hours No receipt of rescue therapies within 3-12 hours from randomization No surgery to decompress the hematoma within 3-12 hours from randomization. Secondary: Percent change from baseline in anti-factor Xa activity during the first 2 hours from randomization Safety Endpoints (assessed at 30 days) Thrombotic events (ischemic stroke, myocardial infarction, VTE). Death Intervention: Andexanet alfa high-dose or low-dose bolus followed by infusion depending on time and dose from last DOAC use. Control: Usual care Design: Non-blinded, randomized controlled trial performed at 131 centers across 23 countries over 4 years. Exclusions GCS < 7 at the time of consent NIHSS > 35 Surgery planned within 12 hours of enrollment Thrombotic event within 2 weeks of enrollment Time from symptom onset > 6 hours Pregnancy Results: Primary results 581 patients were assessed for eligibility across 131 sites over 4 years 31 excluded prior to randomization 20 excluded after randomization due to consent issues 530 analyzed for the safety outcomes 263 patients assigned to andexanet alfa arm 267 patients assigned to usual care arm 452 patients were analyzed for the primary outcome 85.5% (195/228) patients in the usual care arm received 4F-PCC 78.1% (175/224) patients in the andexanet arm received the low-dose regimen Critical Results Andexanet alfa Usual Care Difference (95% CI) P Value Primary Outcome Hemostatic Efficacy 67% (150/224) 53.1% (121/228) 13.4 (4.6 – 22.2) 0.003 NIHSS change < 7 points 87.9% (188/214) 83.0% (181/218) 4.6 (-2.0 – 11.2) Secondary Outcome Anti-Factor Xa % Change -94.5% (-96.6 – 88.9) -26.9% (-54.2 – -9.5) Safety Outcome Thrombotic Events 10.3% 5.6% 4.6 (0.1 – 9.2) 0.048 TIA 0 0 Ischemic Stroke 6.5% 1.5% Myocardial Infarction 4.2% 1.5% DVT 0.4% 0.7% PE 0.4% 2.2% Arterial Embolism 1.1% 0.7% Death 27.8% 25.5% 0.51 Strengths: This is the first randomized trial comparing andexanet alfa to standard care in this patient group. Multicenter, multinational study increasing applicability of findings. Outcome assessors were blinded to treatment arm. Hematoma measurements were made with a standard protocol and central site adjudication. 12 hour NIHSS assessments were performed by health care professionals who were unaware of group assignments Limitations: Study funded, designed, and supervised by AstraZeneca Pharmaceuticals the maker of Andexanet alpha.  Although, this does not refute the findings of this study, it should make readers skeptical. Clinicians were not blinded to the treatment arm patients were randomized to. This may introduce bias particularly in terms of subsequent treatments (treatments outside of reversal are not detailed in the study). Primary endpoint is not patient centered. Convenience sample of patients which introduces bias. There are some baseline differences between groups and it’s hard to say how this may have influenced the results. Exclusion criteria are likely to be difficult for clinicians to assess real time leading to protocol violation (particularly items like planned surgery and recent thrombotic event). Dose adjustment for time from ingestion likely to lead to protocol violation as this info difficult to assess. Exclusion criteria: Removed the sickest patients. Discussion: The positive primary and secondary outcomes Both the primary (hematoma expansion) and secondary (anti-fac

Take Home Points: There are many causes of neutropenia, chemotherapy being by far the most dangerous. Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality. For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but do not wait to initiate treatment. Check old blood cultures and obtain new cultures prior to starting treatment. Identify low risk patients and send them home with PO antibiotics and close oncology follow-up in conjunction with your oncologist. REBEL Core Cast 122.0 – Neutropenic Fever Click here for Direct Download of the Podcast. Neutropenia and Neutropenic Fever Neutropenia: An absolute neutrophil count less than 500 cells/mm3 or less than 1000 cells/mm3 with a predicted decline to less than 500 cells/mm3 ANC = WBC x (neutrophil% + band%) Mild: 1000 – 1500 Mod: 500 – 1000 Severe: 100 – 500 Profound: <100 Background Neutrophils directly combat infection and are important to coordinating the body’s overall immune response. The loss of these cells leads to immunosuppression as well as decreased responsiveness of the immune system as a whole Patients with neutropenia will not only get very sick very quickly, but also will have blunted immune response and may not localize signs of infection well Fever or malaise may be their only presenting symptoms. Patients with hematologic malignancies are at highest risk for suffering profound and prolonged neutropenia. Particularly high risk are those undergoing induction chemotherapy or stem cell transplant. Allogeneic stem cell grafting is higher risk than autologous. Neutropenic Fever:  Fever (one reading of 38.3C or sustained 38.0C) + ANC < 500 cells/mm3 or expected to fall to < 500 cells/mm3 within the next 48 hours Common problem during chemotherapy: 10-50% of patients with solid malignancy and >80% of patients with hematologic malignancy will experience at least one episode of neutropenia (IDSA 2010, Klastersky 2004) Associated with high morality: ~90% without antibiotics (Perron 2014, Klastersky 2009) ~2-21% when treated with early antibiotics (Clarke 2011, Kruderer 2006) Higher mortality rates with co-morbidities and hematologic malignancies Time to antibiotic administration has been shown to directly impact mortality (Perron 2014, Rosa 2014, Marín 2015) Causes of neutropenia (Gibson 2014): Overconsumption Sepsis Autoimmune disease (SLE, rheumatoid arthritis, etc) Underproduction by bone marrow Malnutrition – alcoholism, anorexia, etc Myelodysplastic syndrome Post-viral: varicella, measles, rubella, influenza, hepatitis, Epstein-Barr virus, HIV Drug induced: clozapine, methimazole, sulfasalazine, bactrim, b-lactam antibiotics, NSAIDs, ticlopidine, cephalosporins, chemotherapy Chemotherapy: Includes many drugs and drug regimens, all with the goal of killing rapidly dividing cells. Of note, this particularly affects: Cancer cells – this is the reason chemotherapy works as treatment Neutrophils – with a life cycle of only 1-6 days, their numbers are impacted dramatically by chemotherapy Mucosa – destruction of dividing cells thins mucosal barriers, putting these patients at high risk for mucositis and bacterial invasion This creates a dangerous situation where the body’s barriers against bacterial invasion are broken down and, thus, the ability to combat infection is severely blunted. Antibiotics are effectively the only thing standing between these patients and overwhelming sepsis. Pathogens (Gudiol 2013): The pathogens responsible for neutropenic fever have changed over time. Initially, Gram (-) organisms translocated from the gut caused majority of cases of neutropenic fever This changed in the 1990s. Gram(+) infections became more common due to more fluoroquinolone prophylaxis against Gram (-) organisms and due to more prevalent use of indwelling catheters for outpatient treatment Over the past decade, there has been a resurgence of Gram (-) organisms due to increasing antibiotic resistance, particularly multidrug resistant E coli and klebsiella Given the increasing rates of antibiotic resistance, antibiotic stewardship is becoming increasingly important In the ED, we can contribute to antibiotic stewardship by checking old cultures and obtaining new ones prior to initiation of antibiotics ED Evaluation  and Management: Resuscitate if necessary Patients with neutropenic fever may rapidly progress to septic shock. Give appropriate fluids, vasopressors, and antibiotics. Antibiotics need to be given as quickly as possible if unstable Perform a complete review of systems and physical exam looking for signs of focal infection Basic Blood Work CBC, BMP, LFTs, bilirubin levels Blood cultures If indwelling catheter present: 1 set from each line of indwelling catheter + 1 peripheral set If no indwelling catheter pre

Background: The holy grail of outcomes in OHCA is survival with good neurologic outcome.  The only interventions proven to increase this outcome are high quality CPR and defibrillation in shockable rhythms.  Ventilation is also an important component of resuscitation in OHCA.  Excess minute ventilation can adversely affect hemodynamics due to increased intrathoracic pressure (i.e. decreased venous return). Additionally, low CO2 levels from hyperventilation can lead to cerebral vasoconstriction which could lead to worsened secondary brain injury.       Most organizations recommend adults to be ventilated with tidal volumes of 500 to 600mL/breath during ongoing CPR.  Large adult BVMs can have maximum tidal volumes of ≈1500mL and deliver about 750mL per one handed ventilation.  Simulation studies have shown that health care professionals often provide minute ventilation well above these recommended ranges.       One of the recommendations from many experts to mitigate the perceived risk of large adult BVMs is using smaller adult BVMs.  This change would result in decreasing the maximum volume from 1500 to 1000mL and an expected delivered tidal volume from 750 to 450mL/breath  (much more inline with recommended ranges). However, evidence that this approach makes is difference is lacking. REBEL Cast 126: Should We Not Be Recommending Small Adult BVMs in OHCA? Click here for Direct Download of the Podcast Paper: Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062 Clinical Question: Is large adult BVM or small adult BVM associated with more ROSC in adult patients treated with advanced airway placement for nontraumatic OHCA? What They Did: Retrospective, observational cohort analysis of prospectively obtained data from a single urban EMS system Evaluating adults treated with advanced airway placement for nontraumatic OHCA Jan 2015 to Dec 2021 Changed from large adult BVMs to small adult BVMs in summer of 2017 (3 month crossover period was allowed and excluded from analysis) Used a Mercury medical CPR-2 small ventilation bag Compared rates of ROSC, ventilation rate, and mean end tidal carbon dioxide (ETCO2) by minute before and after small adult BVM implementation Outcomes: Primary: ROSC at the end of EMS care (i.e. Arrival to ED or terminated efforts in the field) Secondary: Ventilation rate Mean end-tidal CO2 (ETCO2) during CPR Inclusion: Adult patients with nontraumatic OHCA Treated with an advanced airway (i.e. Endotracheal intubation or iGel) Exclusion: Age <18 years Received basic life support only Termination of resuscitation due to advanced directives ALS interventions prior to EMS arrival Insufficient capnography data Cricothyrotomy Advanced airway placed while patient had spontaneous circulation Airway was managed with BVM only Did not receive CPR while under EMS ALS care Results: 1994 Patients included in analysis 1331 (67%) treated with small adult BVM 663 (33%) treated with large adult BVM 21% had an initial shockable rhythm ROSC Small Adult BVM: 33% Large Adult BVM: 40% uOR 0.74; 95% CI 0.61 to 0.90; P = 0.003 After adjustment for age, sex, witnessed arrest, bystander CPR, and initial rhythm this finding remained statistically significant (aOR 0.74; 95% CI 0.61 to 0.91) Ventilation rates did not differ between cohorts (≈12BPM) ETCO2 Small Adult BVM: 36.9 +/- 19.2mmHg Large Adult BVM: 33.2 +/- 17.2mmHg P <0.01 Strengths: Written records are compared to cardiac monitor files and audio recordings to adjudicate differences before integrating information into the registry Intubations confirmed with ETCO2 Took into account the COVID-19 pandemic time period Also took into account the potential for trends over time by visualizing the incidence of ROSC by month over a seven year period and found no significant change in the slope before and after the implementation of the small adult BVM Limitations: Only included patients that were intubated with an endotracheal tube or iGel (these results may not apply in patients without these devices) There were some confounding baseline differences (explained more in discussion) Unclear what other interventions were performed in terms of ACLS medications or what the specific causes of the cardiac arrest were from This was a before and after study not allowing for a control group. Before and after studies can introduce numerous biases particularly if other pieces of care changed between the two time periods. (Can also go in the discussion) The actual tidal volume delivered was not measured in this trial and therefore the delivered minute ventilation is unknown As this is a retrospective study, we can only show association, BUT NOT causation of the size of the adult BVM affecting ROSC outcomes Discussion: There are some key BASELINE DIFFERENCES that could

Take Home Points Acute rhinosinusitis is a clinical diagnosis The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement. REBEL Core Cast 121.0 – Acute Sinusitis Click here for Direct Download of the Podcast. Definition: Acute rhinosinusitis (ARS) – Symptoms for less than four weeks Subacute rhinosinusitis – Symptoms for 4 to 12 weeks Chronic rhinosinusitis – Symptoms persisting greater than 12 weeks Recurrent acute rhinosinusitis – Four or more episodes of ARS per year, with interim symptom resolution Epidemiology: (Anon 2004) 20 million cases of sinusitis annually in the US, costing $3.5 billion/year Source of 1 in 5 antibiotic prescriptions for adults Presentation: Sinusitis is most commonly diagnosed by clinical symptoms Common symptoms Purulent nasal discharge Nasal congestion Facial pain or pressure, especially over a sinus or unilaterally Anosmia Hyposmia Fever Cough Fatigue Maxillary pain Ear pressure or fullness. Classification of Sinusitis: ●Acute viral rhinosinusitis (AVRS) ARS with viral etiology (i.e. rhinovirus, influenza, and parainfluenza) Most common form of ARS ●Uncomplicated acute bacterial rhinosinusitis (ABRS) ARS with a bacterial etiology without clinical evidence of extension outside the paranasal sinuses and nasal cavity Bacterial superinfection: 0.5-2% of all ARS ●Complicated acute bacterial rhinosinusitis ARS with bacterial etiology with clinical evidence of extension outside the paranasal sinuses and nasal cavity Sinusitis: Viral vs. Bacterial: Color change in sputum does not determine whether infection is viral or bacterial Viral infections Tend to begin resolution by 7-10 days Rarely have associated fevers If fever present, usually only in the first 48 hours. Guidelines for diagnosing ABRS are Presence of URI/cold symptoms that Don’t improve after 10 days Worsen after 5-7 days of improvement Severe symptoms including high fever, purulent discharge or facial pain for 3-4 days The Data Behind Antibiotic Use Clinically diagnosed acute sinusitis Multiple studies show the same cure rate at 7 days, but improved cure rate at 7-14 days for those who use antibiotics (Lemiengre 2012, Berg 1986, Gwaltney 1996) Overall Treatment Effect NNT = 18 Overall Harm NNH = 8 (mostly GI side effects) Radiographically-diagnosed acute sinusitis (Ahovuo-Saloranta 2008) Endpoint: clinical cure at 7-15 days NNT = 15 NNH = 8 IDSA Recommendations for Antibiotic Treatment (Chow 2012) Patients that should be treated Persistent symptoms w/o improvement (> 10 days) Severe symptoms (> 3-4 days) Worsening (“double-sickening”) (> 3-4 days) Antimicrobials 1st Line Amoxicillin 875 mg PO BID X 5-7 days Doxycycline 100 mg PO BID X 5-7 days 2nd Line Amoxicillin/Calvulanate 875/125 mg PO BID X 5-7 days Levofloxacin 500 mg PO Q24 X 5 days Bottom Line: Given the risk for adverse events associated with antibiotic use, the growing specter of resistance and the lack of significant differences in outcomes with antibiotic use, it is better to avoid antibiotics in most patients with ARS. Antibiotics should be considered in those with severe disease and in immunocompromised patients Take Home Points Acute rhinosinusitis is a clinical diagnosis The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement. References Anon JB et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004; 130(Suppl 1): 1-45. PMID: 14726904 Lemiengre MB et al. Antibiotics for Clinically Diagnosed Acute Rhinosinusitis in Adults. Cochrane Database Syst Rev 2012. PMID: 23076918 Berg O et al. Occurence of asymptomatic sinusitis in common cold and other acute ENT-infections. Rhinology 1986; 24(3): 223-5. PMID: 3775189 Gwaltney JM. Acute community-aquired sinusitis. Clin Infect Dis 1996; 23(6): 1209-23. PMID: 8953061 Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev 2008. PMID: 18425861 Chow AW et al. IDSA Clinical practice guideline for acute bacterial rhino sinusitis in children and adults. Clin Infect Dis 2012; 54(8): e72-e112. PMID: 22438350 Read More The NNT.com: Antibiotics for Clinically Diagnosed Acute Sinusitis in Adults The NNT.com: Antibiotics for Radiologically-Diagnosed Acute Maxillary Sinusitis Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 121.0 – Acute Sinusitis appeared first on REBEL EM - Emergency Medicine Blog.

Podcast Direct Download: Link Release Date: April 16th, 2024 Show Notes The Visible Voices Podcast Dr. Glaucomflecken: Power of Ultrasound with Emergency Medicine Dr. Resa Lewiss Adaira I Landry MD Resa E Lewiss MD is a Professor of Emergency Medicine at the University of Alabama at Birmingham. A TEDMED speaker and TimesUp Healthcare founder, she’s an internationally renowned point-of-care ultrasound educator and champion for diverse, equitable, and inclusive workplaces. She attended college at Brown, medical school at Penn, Emergency Medicine residency at Harvard, and fellowship at Mount Sinai St. Luke’s Roosevelt.  She led point-of-care ultrasound sections at St. Luke’s Roosevelt, the University of Colorado, and Thomas Jefferson. A physician healthcare design consultant for Perkins&Will, her design focus has been ultrasound hardware and workflows. She’s helped to redesign the built environment of a Harvard ICU and an infectious diseases unit in Malawi. As host and founder of the Visible Voices Podcast, she’s interviewed dozens of subject matter experts in healthcare, equity, and current trends. Her writings are published in the popular press and scientific journals, such as Harvard Business Review, Slate, Nature, and Fast Company. Her new book, MicroSkills : Small Actions, Big Impact is forthcoming from HarperCollins in 2024. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL EM Book Club – MicroSkills appeared first on REBEL EM - Emergency Medicine Blog.