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A tartalmat a Salim R. Rezaie, MD, Salim R. Rezaie, and MD biztosítja. Az összes podcast-tartalmat, beleértve az epizódokat, grafikákat és podcast-leírásokat, közvetlenül a Salim R. Rezaie, MD, Salim R. Rezaie, and MD vagy a podcast platform partnere tölti fel és biztosítja. Ha úgy gondolja, hogy valaki az Ön engedélye nélkül használja fel a szerzői joggal védett művét, kövesse az itt leírt folyamatot https://hu.player.fm/legal.
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A tartalmat a Salim R. Rezaie, MD, Salim R. Rezaie, and MD biztosítja. Az összes podcast-tartalmat, beleértve az epizódokat, grafikákat és podcast-leírásokat, közvetlenül a Salim R. Rezaie, MD, Salim R. Rezaie, and MD vagy a podcast platform partnere tölti fel és biztosítja. Ha úgy gondolja, hogy valaki az Ön engedélye nélkül használja fel a szerzői joggal védett művét, kövesse az itt leírt folyamatot https://hu.player.fm/legal.
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Take Home points : Always suspect an open joint if there is a laceration, regardless of size, the lies over joint CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances. Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients REBEL Core Cast 131.0 – Traumatic Arthrotomy Click here for Direct Download of the Podcast . Definition: a deep laceration that extends into the joint capsule, exposing the intra-articular surface to the environment A laceration into the joint exposes the normally sterile intra-articular contents to external contamination Inoculation of the joint often results in septic arthritis Physical Exam: Laceration over joint (can be variable in size) Local wound exploration may be sufficient in identifying the open joint Exam findings suspicious for joint capsule involvement: Air bubbles Extravasation of joint fluid – straw colored, viscous, sometimes oily in appearance Diagnostic testing: Imaging: X-ray Limited ability to see air in joints but a reasonable first test CT scan Intra-articular air visualized on CT ( Konda 2013 ) May be up to 100% sensitive for joint violation Study limited by small numbers, inclusion bias + inadequate gold standard May be considered the standard evaluation modality in many settings. Saline load test Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test. Useful if physical examination equivocal or plain radiographs non-diagnostic Technique ( Video ) Perform arthrocentesis of the joint with a large bore needle (18-20 gauge) Sterile saline is injected into the joint while passive movement is applied to the joint The laceration site is watched for saline extravasation indicating communication between the joint and external environment Sensitivity ranges from 34%-99% depending on the study, joint, and the amount of saline used to load the joint ( Browning 2016 ) Methylene blue Aids in distinguishing a true positive from additional bleeding from the wound Recent studies suggest that the addition of methylene blue does not increase sensitivity if a sufficient amount of saline is used ( Metzger 2012 ) Volume of fluid injected Varies depending on the joint in which you are injecting Higher volumes increase sensitivity but also increase pain for the patient Knee Joint ( Keese 2007 ) 50 ml: Sensitivity of about 46% 194 ml: sensitivity of 95% Elbow Joint ( Feathers 2011 ) 20 ml: Sensitivity of 86% 40 ml: Sensitivity of 95% Ankle Joint ( Bariteau 2013 ) 7 ml: Sensitivity of 50% 30 ml: Sensitivity of 95% ED Management: Reduce open fractures if present Irrigate grossly contaminated wounds in the ED Immobilize the joint to prevent further injury Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours Tetanus prophylaxis Prophylactic antibiotics (best if given within 6 hours) Staph/strep coverage: 1 st generation cephalosporin (i.e. cefazolin or cefuroxime) If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin) If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin) If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn) If seawater contamination and concern for vibrio vulnificus, add doxycycline Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 131.0 – Traumatic Arthrotomy appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating If the patient appears toxic or has systemic symptoms, the simply omphalitis has progressed and aggressive treatment including surgery is likely indicated REBEL Core Cast 130.0 – Omphalitis Click here for Direct Download of the Podcast . Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 130.0 – Omphalitis appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Orogastric lavage may still play an important role in treatment of the overdose patient. Do not perform lavage if the ingestion has limited toxicity at any dose or the ingested dose is unlikely to cause significant toxicity. Strongly consider orogastric lavage in a patient who has taken an overdose of drugs that are particularly toxic, suspected extreme doses associated with high morbidity/mortality and do not have easily available and effective antidotes. Secure the airway prior to placing the lavage tube to minimize aspiration risk. REBEL Core Cast 129.0 – Gastric Lavage Click here for Direct Download of the Podcast . Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 129.0 – Gastric Lavage appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage. Patient who present shortly after ingestion will simply look inebriated – no different than ethanol intoxication. At this point, patients will have an elevated osmolar gap and little to no anion gap. Patient who presents in a delayed fashion after ingestion may have a normal osmolar gap however will manifest the signs of end-organ damage: anion gap metabolic acidosis, visual impairment, or renal dysfunction. The osmolar gap is poorly sensitive, specific surrogate measure that is used to detect the presence of toxic alcohols. A normal osm gap does not rule out a toxic alcohol ingestion. Management includes fomepizole, hemodialysis, and vitamin supplementation. REBEL Core Cast 128.0 – Toxic Alcohols Click here for Direct Download of the Podcast . Reference: Wiener SW. Chapter 106. Toxic Alcohols. 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 October 2, 2024. Guest Expert: Dr. Sanjay Mohan, MD ( Link ) Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 128.0 – Toxic Alcohols appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Anticipate anatomically challenging airways and consider early intubation prior to loss of airway anatomy. Skip the zones of the neck and focus on hard signs of vascular ( Shock w/o another source, Pulsatile bleeding, Expanding hematoma, Audible bruit, Signs of stroke) or aerodigestive (Airway compromise, Bubbling wound, Extensive SubQ air, Stridor, Significant hemoptysis/hematemesis). The presence of hard signs indicates the need to go to the OR or for angiographic intervention. Control hemorrhage with a single finger and direct pressure. REBEL Core Cast 127.0 – Penetrating Neck Injuries Click here for Direct Download of the Podcast . Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 127.0 – Penetrating Neck Injuries appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Early administration of antibiotics (within 60 min) in patients with fever and neutropenia is life saving. Fever in sickle cell is an emergency and always requires cultures and antibiotics even if the child appears well. Avoid sedation and lying supine and steroids in patients with mediastinal masses. Red flags in patients with headaches that may suggest a brain tumor include signs of increased intracranial pressure, focal neurological signs, seizures or ataxia. REBEL Core Cast 126.0 – Peds Hem Onc Emergencies Click here for Direct Download of the Podcast . Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 126.0 – Peds Hem Onc Emergencies appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Always obtain an EKG in patients with ESRD upon presentation Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts In patients who are anuric, early mobilization of dialysis resources is critical REBEL Core Cast 125.0 – Hyperkalemia Click here for Direct Download of the Podcast . Definition: A serum potassium level > 5.5 mmol/L Epidemiology Common electrolyte disorder 10% of hospitalized patients ( Elliott 2010 ) Causes Pseudohyperkalemia: extravascular hemolysis Renal failure (potassium is primarily eliminated by the kidneys) Acidosis Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis) Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine Clinical Manifestations Mild hyperkalemia often asymptomatic Cardiac Effects Increased potassium raises the resting membrane potential of cardiac myocytes Slows ventricular conduction Decreases length of action potential Increases cardiac myocyte excitability Cardiac effects can manifest in lethal dysrhythmias Neuromuscular Effects Paresthesias Weakness Flaccid paralysis Depressed or absent deep tendon reflexes Diagnosis Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD) Serum potassium Can be artificially elevated by extravascular hemolysis Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L 12-Lead EKG Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis) Sensitivity of EKG to detect hyperkalemia is poor ( Wrenn 1991 , Aslam 2002 , Montague 2008 ) Classic EKG findings PR prolongation Peaked T waves Loss of P waves Widening of QRS complex Sine wave Ventricular Fibrillation Asystole Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia ( Mattu 2000 ) Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave) Management Basics: ABCs, IV, O 2 , Cardiac Monitor and, 12-lead EKG Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration) Remove inciting factors (i.e. stop ACEI, NSAIDs etc) Asymptomatic Patients without EKG Changes Eliminate potassium from the body Binding agents (SPS, Sodium zirconium cyclosilicate etc) Enhance renal elimination Intravenous hydration if volume depleted Consider potassium wasting loop diuretics (i.e. furosemide) Dialysis for anuric patients (i.e. ESRD) Symptomatic Patients or Significant EKG Changes Stabilize cardiac myocytes with calcium salts Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization Two Options: CaGluconate, CaCl 2 No difference in time to onset (1 st pass metabolism is a myth) Dose: 1 ampule CaCl 2 (270 mg Ca 2+ ) = 3 ampules CaGluconate (90 mg Ca 2+/ ampule) Onset of action: seconds to minutes Duration: 20-30 minutes Shift potassium into intracellular space (temporary) Insulin (Moussavi 2021) Mechanism: Activation of the Na-K-ATPase Dose: 5-10 units IV Onset of Action: < 15 min Effect: Lowers potassium by about 0.6 mmol Duration of action: 30-60 min Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia Beta-adrenoreceptor agonists (i.e. albuterol) Mechanism: Activation of beta receptors Dose: 10-20 mg inhaled (4-8 standard ampules) Onset of Action: < 15 min Effect: Lowers potassium by about 0.6 mmol Duration of action: 30-60 min Additive effect with insulin ( Allon 1990 ) Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications Sodium Bicarbonate (NaHCO 3 ) Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory ( Elliott 2010 , Weisberg 2008) Eliminate potassium from the body (see above) Asymptomatic Patients with Minor EKG Changes Minimal recommendations on managing this clinical entity Eliminate potassium from the body (see above) Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection Consider medications to shift potassium intracellularly while waiting for elimination Take Home Points Always obtain an EKG in patients with ESRD upon presentation Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts In patients who are anuric, early mobilization of dialysis resources is critical References Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477 Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310 Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216 Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147 Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630 Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671 Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701 Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 125.0 – Hyperkalemia appeared first on REBEL EM - Emergency Medicine Blog .…
 
Take Home Points Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered. REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy Click here for Direct Download of the Podcast . Background and Physiology Shock secondary to beta-blocker (BB) or calcium-channel blocker (CCB) toxicity bears a tremendous degree of morbidity and mortality. According to the 2022 Annual Report of the National Poison Data System from America’s Poison Center, CCBs and BBs account for the sixth and seventh largest number of fatalities from overdose. 1 Recall that cardiac output is a function of both stroke volume and heart rate. The natural response to diminishing stroke volume is a compensatory rise in heart rate (tachycardia). Keep a low threshold to search a patient’s medication list for BB/CCBs, when a hypotension is seen with a “normal heart rate.” Clinical Manifestations Both BBs and CCBs ultimately cause reduced levels of intracellular calcium within myocytes. Depending on the degree of toxicity, subsequent effects include: decreased systemic vascular resistance, vasodilation, bradycardia, various conduction delays, and ultimately hypotension and cardiogenic shock. In addition to abnormal vital signs, look for surrogates of poor clinical perfusion: acidemia, lactate, decreasing urinary output Traditional Management Consider GI decontamination to reduce systemic absorption: 1g/kg up to 50g of activated charcoal. Patient must be alert or the airway must be secured as to avoid aspiration. Obtain multiple lines of intravenous access (3 PIVs or triple lumen CVC) and provide a judicious amount of fluids . (more on this below) Pharmacotherapy Calcium Gluconate: 1-3g intravenous Glucagon: 3mg-5mg slow intravenous push. Rapid administration may induce nausea and emesis. Vasopressors as a bridge to… HIET Mechanism of action is still not fully elucidated however several factors are implicated: Insulin augments cardiac contractility by activating “reverse-mode” Na-Ca exchange and subsequently increasing calcium concentration in the sarcoplasmic reticulum. 2 At a resting physiologic state, the heart utilize free fatty acids as its primary energy course. Under stressed conditions, glucose is used instead. Insulin helps to facilitate glucose metabolism. HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr. If glucose <250 mg/dL, administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV. Ask pharmacy to concentrate insulin from 1 unit/mL to 10 units/ml. Patients often succumb to volume overload given pre-existing cardiac disease and the volume of medical resuscitation through their hospital stay. Once HIET is initiated, dextrose and potassium infusions should simultaneously be started to obviate hypoglycemia and hypokalemia Dextrose: 0.5-1 g/kg/hr via D50/D20 Replete potassium to a minimum of 3.5mEq/L A central venous catheter (often a triple lumen) is often needed to emergently replete potassium and provide D50/D20 safely (given its high osmolarity) Serial monitoring of dextrose (q15-30 minutes) and potassium (q1 hour) is critical HIET has been demonstrated to improve perfusion without necessarily increasing SVR/MAP – while MAPs may not markedly increase dramatically in the short term, obtain serial blood gases, lactate, and track urinary output to track perfusion. 3 Hyperinsulinemia Euglycemia Therapy (HIET) for BB/CCB Toxicity Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement. HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr. HIET therapy requires simultaneous dextrose and potassium infusions as insulin will induce hypoglycemia and shift potassium intracellularly. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered. References Gummin DD, Mowry JB, Beuhler MC, et al. 2022 Annual Report of the National Poison Data System ® (NPDS) from America’s Poison Centers ® : 40th Annual Report. Clin Toxicol (Phila) . 2023;61(10):717-939. doi:10.1080/15563650.2023.226898 von Lewinski D, Bruns S, Walther S, Kögler H, Pieske B. Insulin causes [Ca2+]i-dependent and [Ca2+]i-independent positive inotropic effects in failing human myocardium. Circulation . 2005;111(20):2588-2595. doi:10.1161/CIRCULATIONAHA.104.497461 Holger JS, Engebretsen KM, Fritzlar SJ, Patten LC, Harris CR, Flottemesch TJ. Insulin versus vasopressin and epinephrine to treat beta-blocker toxicity. Clin Toxicol (Phila) . 2007;45(4):396-401. doi:10.1080/15563650701285412 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy appeared first on REBEL EM - Emergency Medicine Blog .…
 
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-factor Xa reduction) outcomes were better in the andexanet group. Unfortunately, these are disease-oriented outcomes instead of patient centered outcomes: the patient doesn’t care if their hematoma expands by 20% or 25% or 30%. They care about clinically important outcomes like disability or death. The authors note that in other studies, hematoma expansion has been associated with worse outcomes, but this was clearly not demonstrated in this study as 90d mRS and death were the same between groups. Bottom line is that there wasn’t even a hint of improved clinical outcomes in the andexanet group. Safety outcomes favored the usual care group In general, larger studies or registries of patients are required to determine safety of a treatment. In this study, however, there is a clear signal for harm even with a small group of patients under ideal circumstances (ie enrolled within a study). Though death was not statistically different, the raw numbers favor usual care. Thrombotic events were clearly increased in the andexanet group. Across a larger group of patients outside of the pristine setting of a study, it is likely that we would see an increase in thrombotic events and death. Only 85.5% of patients in the usual care group received 4F-PCC Though there isn’t abundant evidence for the use of 4F-PCC in this setting, it does represent standard practice. The authors do not report about the subgroup of patients who did not receive 4F-PCC and their outcomes. If this data shows worse outcomes with no reversal treatment, it would suggest that usual care with 4F-PCC may be superior to andexanet alfa for clinical outcomes. If this data shows improved outcomes with no reversal treatment, it would suggest that specific reversal agents aren’t necessary. There were multiple protocol changes during the study. Typically, protocols should not be changed while the study is enrolling patients. This is often done to try to steer the data towards benefit. Initial power calculation was for 900 patients to achieve a 90% power to detect and absolute difference of 10% points in terms of hemostatic efficacy but then made an addendum to the protocol to stop after 450 patients. After this stop point, the safety and monitoring board recommended the trial be stopped. Though the authors state they had no knowledge of the effect prior, there is no clear explanation given for this change and it raises the possibility that the trial was stopped prior to additional data showing harm was collected. Drug cost Andexanet alfa costs between $30 – 50,000/treatment. This only takes into account drug costs (ie not monitoring, nursing costs etc). 4F-PCC costs around $5-6,000/treatment. Author Conclusion: “Among patients with intracerebral hemorrhage who were receiving factor Xa inhibitors, andexanet resulted in better control of hematoma expansion than usual care but was associated with thrombotic events, including ischemic stroke.” Clinical Take Home Point: The authors conclusions are correct. However, they don’t properly stress the findings. Treatment of patients with intracerebral hemorrhage on a DOAC with Anexanet alfa did not improve clinical outcomes when compared to usual care. Based on safety data, andexanet alfa resulted in increased harm to patients. Andexanet alfa should not be part of the standard treatment in this scenario based on the available evidence. References: Greenberg SM et al. 2022 Guidelines for the Management of Patients with Spontaneous Intracerebral Hemorrhage: A Guideline from the American Heart Association/American Stroke Association. Stroke 2022; 53(7). PMID: 35579034 Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032 For More Thoughts on This Topic Checkout: REBEL EM: ANNEXA-4 – Andexanet Alfa and Factor Xa Inhibitors First10EM: Andexanet Alfa – More Garbage Science in the New England Journal of Medicine EM Lit of Note: Disutility, thy Name is ANEXXA-4 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal appeared first on REBEL EM - Emergency Medicine Blog .…
 
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/mm 3 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/mm 3 or expected to fall to < 500 cells/mm 3 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 present: 2x peripheral sets Additional testing based on signs and symptoms: Respiratory symptoms CXR Sputum cultures Dysuria Urinalysis Urine culture Abdominal pain CT abdomen and pelvis If diarrhea present, consider C difficile PCR (if available) Isolation Good hand hygiene is the most effective way to prevent these patients obtaining nosocomial infections Use standard barrier precautions Keep anyone with potentially communicable illness out of the patient’s room – visitors, other patients, or healthcare workers No plants in the treatment room or nurse’s station Any stem cell transplant patient should be in a private room. If they have an allogenic transplant, use a HEPA filter with >12 air exchanges per hour Isolation is important for neutropenic patients, but do not let waiting on an isolation room delay obtaining cultures and initiating antibiotics Specific Pathologies Mucositis Mucositis is a high risk feature indicative of bacterial invasion through thinned mucus membrane barriers. Signs and Symptoms oral pain, erythema, edema, or lesions sinus pain or pressure rectal pain or lesions, any swelling suggestive of perirectal abscess abdominal pain Inspect the rectum for swelling possibly indicative of perirectal abscess. Digital rectal exam is generally discouraged due to concern of inducing bacteremia if mucus membranes are damaged in the process Neutropenic Enterocolitis (Typhlitis): A feared complication of neutropenic fever is direct bacterial invasion of the intestinal mucosa causing necrotizing infection Most commonly at the ileocecal junction It presents with classic triad of neutropenia, fever, and RLQ pain . Mortality approaches 50% when present ( Gorschlüter 2005 ) Surgery is avoided unless the bowel perforates, as these patients have poor wound healing and high surgical complication rates Determine whether the patient is high or low risk: High Risk Factors: HD instability Hematologic malignancy Uncontrolled or widespread malignancy Induction chemotherapy / hematopoietic stem cell transplant ANC <100 >7 days of ANC <500 Medical comorbidities (particularly COPD, cardiac disease, or diabetes) Low Risk Factors: HD stable Solid tumor malignancy ANC >500 Neutropenia expected to last <7 days No comorbidities MASCC and CISNE risk calculators: MASCC Score Low risk = 21-26 High risk = <21 The MASCC Score will identify more patients as low risk, but will have more treatment failures / bounce-backs than the CISNE score ( Ahn 2017 , Coyne 2016 ) CISNE Score Low risk = 0 Intermediate risk = 1-2 High risk = 3-8 The CISNE score will identify fewer patients as low risk, but will result in fewer treatment failures/bounce-backs than the MASCC score ( Ahn 2017 , Coyne 2016 ) . Default to using whichever score your oncologist is more comfortable with. Antibiotic Selection Check old cultures for prior infections and sensitivities (if available). Follow your hospital’s protocol (if available). This will have been formulated based on local resistance patterns and likely with input from your institution’s oncologists. High Risk Patients will need hospitalization and IV antibiotics. General approach for IV antibiotic therapy: Begin with single broad spectrum agent which includes pseudomonas coverage such as cefepime, piperocillin-tazobactam, or a carbepenem Penicillin allergies other than anaphylaxis are not considered a contraindication to the use of cephalosporins such as cefepime If patient has anaphylactic reaction to penicillins, consider broad coverage with ciprofloxacin plus clindamycin or aztreonam plus vancomycin ( IDSA 2010 ) Do not routinely start vancomycin. Add vancomycin if there is clinical suspicion for Gram (+) infection Signs of mucositis or cellulitis Indwelling catheter present on arrival Prior MRSA infection Patient already on Gram (-) prophylaxis such as fluoroquinolone Consider adding additional agents for unstable patients, or patients in which antibiotic resistant organisms are suspected (patient has known colonization or patient population has high endemic rates). MRSA: vancomycin, linezolid, or daptomycin VRE: linezolid or daptomycin Extended spectrum beta lactamase (ESBL) producing organisms: carbapenem Carbapenemase producing organisms (such as klebsiella): polymixin-colistin or tigecycline If there is clinical suspicion for influenza (or positive PCR testing), treatment with oseltamivir is recommended Other antiviral and antifungal agents should NOT be started routinely. Only start antiviral or antifungal therapies if the patient has a known viral or fungal infection (ex: patient spikes a fever while already on antifungal treatment) or if they have a clinical picture strongly suggestive of viral or fungal etiology Antifungals are generally not initiated until a patient has had >4 days of fever unresponsive to antibiotic treatment with no clear source identified Low risk If the patient has no high risk features, is found to be low risk on MASCC or CISNE scoring, and has good oncology follow-up, it may be preferable to discharge them home with 24hr oncology follow-up Send patients home ONLY after discussion with the patient’s oncologist and only if there are no high risk features present Outpatient antibiotic choice: Ciprofloxacin plus amoxicillin-clavulanate is recommended by IDSA guidelines for oral empiric therapy ( IDSA 2010 ) Levofloxacin or ciprofloxacin monotherapy, or ciprofloxacin plus clindamycin are less well studied but are commonly used Avoid fluoroquinolones if the patient is already on fluoroquinolone prophylaxis 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. Read More: Infectious Disease Society of America 2010 Clinical Practice Guidelines Life in the Fast Lane: Febrile Neutropaenia Uptodate: overview of neutropenic fever syndromes EMRAP: Risk stratification of neutropenic fever MDCalc: MASCC Score MDCalc: CISNE Score References: Ahn S, Rice TW, Yeung SJ, Cooksley T. Comparison of the MASCC and CISNE scores for identifying low-risk neutropenic fever patients: analysis of data from three emergency departments of cancer centers in three continents. Support Care Cancer. 2018 May;26(5):1465-1470. doi: 10.1007/s00520-017-3985-0. Epub 2017 Nov 22. Clarke, R. T., Warnick, J., Stretton, K., Littlewood, T. J., Improving the immediate management of neutropenic sepsis in the UK: Lessons from a national audit. British Journal of Haematology. 2011 Jun;153(6):773-9. doi: 10.1111/j.1365-2141.2011.08693.x. Epub 2011 Apr 22 Coyne CJ, Le V, Brennan JJ, Castillo EM, Shatsky RA, Ferran K, Brodine S, Vilke GM. Application of the MASCC and CISNE Risk-Stratification Scores to Identify Low-Risk Febrile Neutropenic Patients in the Emergency Department. Ann Emerg Med. 2017 Jun;69(6):755-764. doi: 10.1016/j.annemergmed.2016.11.007. Epub 2016 Dec 29. Ellis M. Febrile Neutropenia. Annals of New York Academy of Sciences. 2008 Sep;1138:329-50. doi: 10.1196/annals.1414.035. Freifeld, A. G., Bow, E. J., Sepkowitz, K. A., Boeckh, M. J., Ito, J. I., Mullen, C. A., Raad, II, et al., Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the infectious diseases society of america, Clinical Infectious Diseases, 2011, 52(4):e56-93. Gibson C, Berliner N. How we evaluate and treat neutropenia in adults. Blood. 2014 Aug 21;124(8):1251-8; quiz 1378. doi: 10.1182/blood-2014-02-482612. Epub 2014 May 28. Gorschlüter M, Mey U, Strehl J, et al. Neutropenic enterocolitis in adults: systematic analysis of evidence quality. Eur J Haematol 2005; 75:1. Gudiol C, Bodro M, Simonetti A, et al. Changing aetiology, clinical features, antimicrobial resistance, and outcomes of bloodstream infection in neutropenic cancer patients. Clin Microbiol Infect 2013; 19:474 Klastersky J. The changing face of febrile neutropenia-from monotherapy to moulds to mucositis. Why empirical therapy? J Antimicrob Chemother. 2009;14(Suppl 1):i14–i15 Klastersky J. Management of fever in neutropenic patients with different risks of complications. Clin Infect Dis. 2004;39(Suppl. 1):S32–S37 Kuderer NM, Dale DC, Crawford J, Cosler LE, Lyman GH. Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients. Cancer. 2006 May 15;106(10):2258-66. Marín M, Gudiol C, Ardanuy C, Garcia-Vidal C. Jimenez L, Domingo-Domenech E, Pérez FJ, Carratalà J. Factors influencing mortality in neutropenic patients with haematologic malignancies or solid tumours with bloodstream infection. Clinical Microbiology and Infection. Volume 21, Issue 6, June 2015, Pages 583-590 Perron T, Emara M, Ahmed S. Time to antibiotics and outcomes in cancer patients with febrile neutropenia. BMC Health Services Research . 2014;14:162. doi:10.1186/1472-6963-14-162. Radiologypics, P. B. (2014, November 10). Neutropenic Colitis (Typhlitis). Retrieved from https://radiologypics.com/2014/11/10/neutropenic-colitis-typhlitis/ Rosa RG, and Goldani LZ. Cohort Study of the Impact of Time to Antibiotic Administration on Mortality in Patients with Febrile Neutropenia. Antimicrob Agents Chemother. 2014 Jul; 58(7): 3799–3803. doi: 10.1128/AAC.02561-1 Stiff, PJ. Coding for Mucositis. From presentation at ICD-9-CM Coordination and Maintenance Committee Meeting. Loyola University Medical Center. Centers for Disease Control. September 30, 2005. Retreived from https://www.cdc.gov/nchs/ppt/icd9/att_mucositis_sep05.ppt Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie ) The post REBEL Core Cast 122.0 – Neutropenic Fever appeared first on REBEL EM - Emergency Medicine Blog .…
 
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 account for the results of this trial (i.e. confounders): More patients in the small adult BVM cohort received bystander CPR (64% vs 59%). This would favor more ROSC in the small adult BVM cohort Unwitnessed arrest was slightly greater in the large adult BVM cohort (58% vs 53%)…This would favor more ROSC in the small adult BVM cohort Fewer patients in the small adult BVM cohort arrested in public (22% vs 27%…Unclear how this would impact ROSC The interval from 911 call to start of CPR (10 vs 9min) and advanced airway placement (20 vs 18min) were longer in the small adult BVM cohort…Not sure 1 to 2min of difference would result in more ROSC in the large adult BVM cohort Adherence to guideline recommended ventilation rates of 10 BPM was more common in the small adult BVM cohort (28.4% vs 31.2%)…This would favor more ROSC in the small adult BVM cohort It would appear most things at baseline favored the small adult BVM cohort (Although the authors did account for most of these in adjusted analyses) The end of this trial took place during the COVID-19 PANDEMIC: Anyone who took care of cardiac arrest patients during the COVID-19 pandemic knows that there were significant delays in care According to the authors any cases of OHCA that occurred after the start of the pandemic (Feb 2020) were censored from the analysis and the results were evaluated again When looking at cases of OHCA that occurred prior to Feb 2020 the small adult BVM cohort had a similarly lower odds of ROSC (OR 0.75; 95% CI 0.60 to 0.93; p = 0.008) as the entire time period this intervention was implemented This remained the case even after adjusting for initial rhythm, age, sex, witnessed arrest and bystander CPR (aOR 0.76; 95% CI 0.61 to 0.95; p = 0.018) While I would imagine during a code most people are bagging faster than 10BPM, in this study 6 to 18 BPM were delivered in 82.5% of the measured ventilations. Is this a result of Hawthorne effect or the implementation of a metronome to guide chest compression and ventilation rates (implemented June of 2015) or simply a well trained EMS system? This addition would seem to favor the small adult BVM group This EMS organization appears to be very high functioning with lots of training and education which may not be the standard at other agencies. The fact that the medics are providing a good RR and good TV throughout a 7-year period would suggest this and in doing so a simple change from a large adult BVM to a small adult BVM may have resulted in the association of lower ROSC whereas an agency that does not get as much training or high functioning may actually still be causing harm with the large adult BVM Finally, there was a higher ETCO2 in the small adult BVM cohort compared to the large adult BVM cohort. As ventilatory rate was essentially similar between groups, this most likely means a smaller tidal volume was delivered with each breath. This smaller tidal volume could have lead to physiologic changes that are potentially harmful: Hypoventilation Increased dead space fraction Alveolar decruitment Atelectasis causing shunt physiology Author Conclusion: “Use of small adult bag during OHCA was associated with lower odds of ROSC at the end of EMS care. The effects on acid base status, hemodynamics, and delivered minute ventilation remain unclear and warrant additional study.” Clinical Take Home Point: This is a really messy trial, with lots of methodological and confounding issues that make it difficult to interpret. It does show that when experts recommend an intervention it is important to study it. Until better evidence shows us differently it is probably best to stick with a large adult BVM but use one hand for bagging and maintain a rate of 10BPM. References: 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 Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami ) The post REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? appeared first on REBEL EM - Emergency Medicine Blog .…
 
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 .…
 
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