We review Acute Respiratory Distress Syndrome

Hosts:
Sadakat Chowdhury, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/ARDS.mp3 Download Leave a Comment Tags: Critical Care, Pulmonary

Show Notes

• Definition of ARDS:
  • Non-cardiogenic pulmonary edema characterized by acute respiratory failure.
  • Berlin criteria for diagnosis include acute onset within 7 days, bilateral pulmonary infiltrates on imaging, not fully explained by cardiac failure or fluid overload, and impaired oxygenation with PaO2/FiO2 ratio <300 mmHg, even with positive end-expiratory pressure (PEEP) >5 cm H2O.
• Severity based on oxygenation (Berlin criteria):
  • Mild: PaO2/FiO2 200-300 mmHg
  • Moderate: PaO2/FiO2 100-200 mmHg
  • Severe: PaO2/FiO2 <100 mmHg
• Epidemiology:
  • Occurs in up to 23% of mechanically ventilated patients.
  • Mortality rate of 30-40%, primarily due to multiorgan failure.
• Differentiation from Cardiogenic Pulmonary Edema:
  • Chest CT shows diffuse edema and pleural effusion in cardiogenic edema; patchy edema, dense consolidation in ARDS.
  • Ultrasound may show diffuse B lines in cardiogenic edema; patchy B lines and normal A lines in ARDS.
• Pathophysiology:
  • Exudative phase: Immune-mediated alveolar damage, pulmonary edema, cytokine release.
  • Proliferative phase: Reabsorption of edema fluid.
  • Fibrotic phase: Potential for prolonged ventilation.
• Etiology:
  • Direct lung injury (pneumonia, toxins, aspiration, trauma, drowning) and indirect causes (sepsis, pancreatitis, transfusion reactions, certain drugs).
• Diagnostics:
  • Comprehensive workup including imaging (chest X-ray, CT), laboratory tests (complete blood count, basic metabolic panel, blood gases), and specialized tests depending on suspected etiology.
• Management Strategies:
  • Steroids: Beneficial in certain etiologies of ARDS, with specifics on dosing and duration.
  • Fluid Management: Conservative fluid strategy, diuresis guided by patient condition.
  • Ventilation: Non-invasive ventilation (NIV) preferred in specific cases; mechanical ventilation strategies to ensure lung-protective ventilation.
  • Proning: Used in severe ARDS to improve oxygenation.
  • Inhaled Vasodilators: Used for refractory hypoxemia and specific complications like right heart failure.
  • Extracorporeal Membrane Oxygenation (ECMO): Considered for severe ARDS as salvage therapy.
  • Supportive Care: Includes monitoring and management of complications, nutrition, and physical therapy.
• Ventilation Specifics:
  • Tidal volume and pressure settings aim for lung-protective strategies to prevent ventilator-induced lung injury.
  • Permissive hypercapnia, plateau pressure, PEEP, and ventilation mode adjustments based on patient response.
  • ARDSnet Table: ventilator_protocol_2008-07

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We review Nitrous Oxide Toxicity: Symptoms, diagnosis, and treatment overview

Hosts:
Stefanie Biondi, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nitrous_Oxide_Toxicity.mp3 Download Leave a Comment Tags: Toxicology

Show Notes

Patient Case Illustration

• Hypothetical case: 21-year-old male with no previous medical history, experiencing a month of progressively worsening numbness, tingling, and weakness. Initially starting in his toes and spreading to his hips, and later involving his hands, the symptoms eventually escalated to the point of immobilization. Despite initially denying drug use, the patient admitted to using 40-60 canisters of nitrous oxide (whippets) every weekend for the last three months.

Background and Recreational Use of Nitrous Oxide

• Nitrous oxide, a colorless, odorless gas with anesthetic properties.
• Synthesized in the 18th century.
• Its initial medical purpose expanded into recreational use due to its euphoric effects.
• Resurgence as a recreational drug during the COVID-19 lockdowns.
• Accessibility and legal status.

Public Misconceptions and Health Consequences

• There are widespread misconceptions about nitrous oxide
  • Particularly the belief in its safety and lack of long-term health risks.
  • Contrary to popular belief, frequent use of nitrous oxide can lead to significant, sometimes irreversible, health issues.

Neurological Examination and Diagnosis

• Key components of the examination include assessing strength, sensation, cranial nerves, and proprioception, with specific abnormalities such as symmetrically decreased strength in a stocking-glove pattern, upgoing Babinski reflex, and positive Romberg sign being indicative of potential toxicity. 

Physical Exam Findings: Upper vs Lower Motor Neuron Lesions

Localize the Lesion- Differential Diagnoses for Extremity Weakness 

Localize the Lesion- Differential Diagnoses for Extremity Weakness

Localize the Lesion- Differential Diagnoses for Extremity Weakness

MRI Findings and Subacute Combined Degeneration

• The MRI displayed symmetric high signal intensity in the dorsal columns, a diagnostic feature identified as the inverted V sign or inverted rabbit ear sign.
• Significance of the Inverted V Sign: This MRI sign is pathognomonic for subacute combined degeneration, indicating it is a distinct marker for this condition.
• T2 Weighted Axial Images: The inverted V sign is observed in T2 weighted axial MRI images, which are used to evaluate the presence and extent of demyelination within the spinal cord.
• Interpretation of Hyperintense Signals: Hyperintense signals on T2 weighted images generally indicate demyelination, where the protective myelin sheath around nerve fibers is damaged or destroyed.
• Anatomical Location: The dorsal columns, located anatomically dorsal (toward the back) within the spinal cord, will appear toward the bottom of the screen in an axial (cross-sectional) view on the MRI.
• Demyelination Appearance: Demyelination in the dorsal columns, typically situated in the thoracic spine, manifests as an upside-down V shape on the MRI, correlating with the described inverted V or rabbit ear sign.

Pathophysiology of SCD due to Nitrous Oxide

• Nitrous Oxide’s Effect on Vitamin B12: Nitrous oxide inactivates vitamin B12 by oxidizing a cobalt component within the molecule, rendering the vitamin functionally ineffective despite adequate consumption and absorption.
• Impact on Methionine Synthase: The oxidation of vitamin B12 by N2O prevents it from activating methionine synthase, an enzyme critical for important biochemical processes.
• Folate to Tetrahydrofolate Conversion: Inactive methionine synthase cannot convert folate into tetrahydrofolate, which is necessary for DNA synthesis. This disruption can lead to megaloblastic anemia, a condition associated with N2O-induced subacute combined degeneration.
• Conversion of Homocysteine to Methionine: Methionine synthase is also responsible for converting homocysteine to methionine. Methionine is essential for the maintenance of myelin integrity, the protective sheath around nerve fibers.
• Demyelination and Neurological Symptoms: The inability to maintain myelin integrity due to disrupted methionine production leads to the demyelination of dorsal columns and peripheral motor/sensory nerves, characteristic of N2O-SCD.
• Normal B12 Levels with Functional Deficiency: Blood levels of vitamin B12 can appear normal in individuals affected by N2O exposure, as the issue lies in the vitamin’s inactivation rather than its absence, creating a functional deficiency.
• Diagnosis of N2O-SCD: To diagnose N2O-induced SCD, healthcare providers need to check for elevated levels of methylmalonic acid and homocysteine. These substances are typically metabolized with the help of vitamin B12, and their elevated levels indicate a functional deficiency of B12 due to N2O exposure.

Treatment and Management

• Lack of Standardized Treatment: There is no universally accepted treatment protocol for N2O induced SCD, but common practices exist based on neurologist recommendations.
• B12 Injection Protocol: A common approach involves administering vitamin B12 injections daily or every other day until there is noticeable improvement in symptoms. Once symptoms start to improve, the frequency of injections can be reduced to once a week.
• Importance of Abstinence from N2O: For recovery to be possible, it is crucial that the patient completely abstains from using whippets (recreational N2O canisters). Continuing to use N2O can inactivate the administered vitamin B12, undermining the treatment efforts.
• Recovery Process: Recovery from N2O induced SCD is typically slow and may not be complete. While remyelination and neurological function can gradually improve, the process is lengthy and may not fully return to baseline.
• Recovery Statistics: Approximately 80% of individuals with N2O-SCD experience some improvement after a year of consistent B12 treatment. However, only between 10% and 20% of patients fully recover to their pre-condition baseline.
• Risk Factors and Prevalence: The risk of developing SCD correlates with the frequency and quantity of N2O use. About 3.4% of individuals who use whippets will develop SCD, with the risk increasing to 8.5% among those who use more than 100 canisters per session. The case in point involved a patient using 20-40 canisters per session.
• Increased Risk with Preexisting Conditions: Individuals who already have a vitamin B12 deficiency are at a greater risk of experiencing SCD symptoms, even with minimal use of whippets. This highlights the importance of understanding individual health conditions and potential vulnerabilities when assessing risk.

Conclusion and Preventive Measures

• Providers should be vigilant in screening for nitrous oxide use among patients presenting with unexplained neurological symptoms. The goal is to enhance early detection and treatment of N2O-induced SCD and to educate patients on the potential long-term health consequences of recreational nitrous oxide use.

References

• Neurology. Mumenthaler M, Mattle H, Taub E, ed. 4th Edition. Stuttgart: Thieme; 2003. doi:10.1055/b-005-148905
• Zayia LC, Tadi P. Neuroanatomy, Motor Neuron. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554616/
• Khin-Htun S, Tan H, Aung T. “Approach to a Patient With Weakness” 2021 Feb 15. Youtube. https://www.youtube.com/watch?v=3WQvtCuC4Fo&t=922s 
• Bhattacharyya S.Spinal Cord Disorders: Myelopathy, The American Journal of Medicine, Volume 131, Issue 11, 2018, Pages 1293-1297, ISSN 0002-9343,https://doi.org/10.1016/j.amjmed.2018.03.009.
• ​​Garg RK, Malhotra HS, Kumar N. Approach to a case of myeloneuropathy. Ann Indian Acad Neurol. 2016 Apr-Jun;19(2):183-7. doi: 10.4103/0972-2327.182303. PMID: 27293327; PMCID: PMC4888679.
• Lim PAC. Transverse Myelitis. Essentials of Physical Medicine and Rehabilitation. 2020:952–9. doi: 10.1016/B978-0-323-54947-9.00162-0. Epub 2019 Apr 17. PMCID: PMC7151963.
• Jayarangaiah A, Lui F, Theetha Kariyanna P. Lambert-Eaton Myasthenic Syndrome. [Updated 2023 Oct 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507891/
• Nguyen TP, Taylor RS. Guillain-Barre Syndrome. [Updated 2023 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532254/
• Froese DS, Fowler B, Baumgartner MR. Vitamin B12 , folate, and the methionine remethylation cycle-biochemistry, pathways, and regulation. J Inherit Metab Dis. 2019 Jul;42(4):673-685. doi: 10.1002/jimd.12009. Epub 2019 Jan 28. PMID: 30693532. 
• Guo CJ, S. Kaufman B. Inhalational Anesthetics. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw-Hill Education; 2019. Accessed February 27, 2024. https://accessemergencymedicine-mhmedical-com.ezproxy.med.nyu.edu/content.aspx?bookid=2569&sectionid=210274345
• Lin JP, Gao SY, Lin CC. The Clinical Presentations of Nitrous Oxide Users in an Emergency Department. Toxics. 2022 Feb 26;10(3):112. doi: 10.3390/toxics10030112. PMID: 35324737; PMCID: PMC8950993. 
• Qudsiya Z, De Jesus O. Subacute Combined Degeneration of the Spinal Cord. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559316/ 
• Hemmer B, Glocker FX, Schumacher M, et alSubacute combined degeneration: clinical, electrophysiological, and magnetic resonance imaging findingsJournal of Neurology, Neurosurgery & Psychiatry 1998;65:822-827.
• Shah K, Murphy C. Nitrous Oxide Toxicity: Case Files of the Carolinas Medical Center Medical Toxicology Fellowship. J Med Toxicol. 2019 Oct;15(4):299-303. doi: 10.1007/s13181-019-00726-x. Epub 2019 Aug 6. PMID: 31388940; PMCID: PMC6825085. 
• Kalmoe MC, Janski AM, Zorumski CF, Nagele P, Palanca BJ, Conway CR. Ketamine and nitrous oxide: The evolution of NMDA receptor antagonists as antidepressant agents. J Neurol Sci. 2020 May 15;412:116778. doi: 10.1016/j.jns.2020.116778. Epub 2020 Mar 19. PMID: 32240970. 
• https://www.nytimes.com/2021/01/30/style/nitrous-oxide-whippets-tony-hsieh.html 

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We review threatened abortion and the complexities in its care.

Hosts:
Stacey Frisch, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Threatened_Abortion.mp3 Download One Comment Tags: OBGYN

Show Notes

Background

• Defined as vaginal bleeding during early pregnancy (before 20 weeks) with a closed cervical os, no passage of fetal tissue, and IUP on ultrasound
• Occurs in 20-25% of all pregnancies.

Initial Assessment and Management

• Priority is to assess patient stability, establish good IV access, FAST may be helpful in identifying some ruptured ectopics early
• Broad differential diagnosis is crucial to avoid mistaking conditions like ectopic pregnancy for other emergencies.
• Importance of a detailed history and physical examination.

Diagnostic Approach

• Essential tests include HCG level, urinalysis, and possibly CBC + blood type/Rh status.
• Rhogam’s use is well-supported in second and third trimester bleeding; however, data is less robust for first trimester bleeding in preventing sensitization
• Importance of interpreting b-HCG with caution and understanding HCG discriminatory zones.
• Use of ultrasound imaging, both bedside and formal, to assess the pregnancy’s status.

Patient Counseling and Management

• Open and honest communication about the prognosis of threatened abortion.
• Addressing psychosocial aspects, including dispelling guilt and myths, and screening for intimate partner violence and mental health issues.
• Recommendations against bedrest and certain activities
• Lack of evidence supporting restrictions on sexual activity.
• Standard pregnancy guidelines: avoiding smoking, alcohol, drug use, and starting prenatal vitamins.

Follow-up and Precautions

• Adopting a wait-and-see approach for stable patients, with scheduled follow-ups for ultrasounds and beta-HCG tests.
• Educating patients on critical warning signs that require immediate medical attention.
• Emphasizing the importance of returning to the hospital if experiencing significant bleeding or other severe symptoms.

Take Home Points

1. Threatened Abortion is defined as Experiencing abdominal pain and/or vaginal bleeding during early pregnancy (before 20 weeks), characterized by a closed cervical os and no expulsion of fetal tissue. In these cases, it is important to assess patient stability promptly.
2. Keep your differential broad in these cases. The evaluation will in most cases involve a combination of labs and ultrasound imaging. 
3. Understand that the Rhogam certainly has a role in second and third trimester vaginal bleeding in the Rh-negative patient, and that there is a dearth of good data on its role in the first trimester – it will ultimately be a decision that is made by you, OBGYN, and the patient. 
4. Approach the interpretation of HCG levels with caution and remember that ectopic pregnancies might not adhere to conventional HCG levels.
5. Established follow up and discharge instructions are crucial.  Manage stable patients with a watchful waiting approach, scheduling subsequent visits for continuous ultrasounds and HCG testing. Clearly outline the importance of immediate medical attention for symptoms such as intense bleeding, significant abdominal pain, fever, or feelings of insecurity at home.
6. Finally, we play an important role wherein we must ensure that the patient is medically stable and psychosocially safe. Here, compassionate communication is crucial when discussing what the diagnosis might entail, alleviate any feelings of blame or shame, and remain vigilant for signs of intimate partner violence or mental health issues.  As emergency medicine physicians, it’s crucial for us to approach these cases with a comprehensive mindset.

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We review a general approach to syncope in children.

Hosts:
Brian Gilberti, MD
Ellen Duncan, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Syncope_in_Children.mp3 Download Leave a Comment Tags: Cardiology, Pediatrics

Show Notes

• Initial Evaluation and Management:
  • Similar initial workup for children and adults: checking glucose levels for hypoglycemia and conducting an EKG.
  • The history and physical exam are crucial.
• Dextrose Administration in Children:
  • Explanation of the ‘rule of 50s’ for determining the appropriate dextrose solution and dosage for children.
• ECG Analysis:
  • Importance of ECG in diagnosing dysrhythmias like long QT syndrome, Brugada syndrome, catecholamine polymorphic V tach, ARVD, ALCAPA, and Wolff-Parkinson-White syndrome.
  • Younger children’s dependency on heart rate for cardiac output and the risk of arrhythmias in kids with congenital heart disease.

Condition Characteristic ECG Findings Congenital/Acquired Long QT Syndrome (LQTS) Prolonged QT interval Congenital/Acquired Wolff-Parkinson-White Syndrome (WPW) Short PR interval, Delta wave Congenital Brugada Syndrome ST elevation in V1-V3, Right bundle branch block Congenital Atrioventricular Block (AV Block) PR interval prolongation (1st degree), Missing QRS complexes (2nd & 3rd degree) Congenital/Acquired Supraventricular Tachycardia (SVT) Narrow QRS complexes, Absence of P waves, Tachycardia Congenital/Acquired Ventricular Tachycardia Wide QRS complexes, Tachycardia Congenital/Acquired Arrhythmogenic Right Ventricular Dysplasia (ARVD/C) Epsilon waves, V1-V3 T wave inversions, Right bundle branch block Congenital Hypertrophic Cardiomyopathy (HCM) Left ventricular hypertrophy, Deep Q waves Congenital Pulmonary Hypertension Right ventricular hypertrophy, Right axis deviation Acquired Athlete’s Heart Sinus bradycardia, Voltage criteria for left ventricular hypertrophy Acquired Catecholaminergic Polymorphic VT (CPVT) Bidirectional or polymorphic VT, typically normal at rest Congenital Anomalous Origin of Left Coronary Artery from Pulmonary Artery (ALCAPA) May be normal, signs of ischemia or infarction in severe cases Congenital

• History Taking:
  • Key aspects include asking about syncope with exertion, syncope after being startled, and syncope after pain or emotional stress.
  • Prolonged loss of consciousness may indicate seizures, and emotional stress and pain can trigger breath-holding spells.
• Breath-Holding Spells:
  • Clarification of misconceptions about breath-holding spells, discussing their causes and characteristics, like cyanotic and pallid types.
  • Association with iron deficiency and the fact that most children outgrow these spells by age 8.
• Physical Examination and History:
  • A cardiac exam is vital, with specific signs to look for, like murmurs in hypertrophic cardiomyopathy.
  • History can help identify the etiology of syncope, such as vasovagal responses or orthostatic hypotension.
• Vasovagal Syncope:
  • Common in kids, especially teenagers, typically presenting with a prodrome of lightheadedness, diaphoresis, and pallor.
  • Normal glucose and EKG are expected in these cases.
• Additional Lab Tests:
  • Pregnancy tests in reproductive-age women, and checking for less common causes like pulmonary embolism, subarachnoid hemorrhage, and toxic exposures.

Take Home Points:

• Immediate assessments for syncope in children should include a FS to evaluate for hypoglycemia and an ECG to evaluate any cardiac rhythm or conduction abnormalities.
• Apply the “Rule of 50s” for hypoglycemic patients to suggest which fluids should be used.
• Refer to our table for ECG findings to look out for when reviewing ECG tracings for these patients.
• Pay particular attention to clues in the history that would suggested HCOM or seizures.
• Breath-holding spells usually resolve by eight
• HCOM murmurs will increase with Valsalva maneuver 
• Always keep your differential broad when approaching these patients given the heterogeneity of potential pathology that could lead to this chief complaint

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We go over the treatment of rapid atrial fibrillation (afib with RVR).

Hosts:
Brian Gilberti, MD
Jonathan Kobles, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Rapid_Atrial_Fibrillation.mp3 Download One Comment Tags: Cardiology

Show Notes

Understanding AF with RVR Categories

• General AF with RVR: Definition and basic understanding.
• Rapid AF with Pre-excitation: Characteristics and complications.
• Chronic AF in Critical Illness: Identification and special considerations.

Stability Assessment in AF with RVR

• ACLS Protocols: Distinction between unstable and stable patients.
  • Unstable Patients: Immediate need for synchronized cardioversion, standard dose at 200 J for adults.
  • Stable Patients: Rate vs. rhythm control strategies, consideration of underlying etiology.
• Limitations in Chronic AF: Challenges in patients with AF secondary to critical illness.

ACLS Guidelines and ECG Findings

• Tachycardia with a Pulse Approach: Initial assessment guidelines.
• ECG Interpretation:
  • Irregularly Irregular Rhythm: Absence of discernible P waves.
  • Ventricular Rate: Typically over 100 bpm.
  • QRS Complexes: Usually narrow, alterations in the presence of bundle branch block or ventricular rate-related aberrancy.
• Identifying Pre-Excitation Syndromes: Signs of shortened PR interval and slurred QRS, indication of Wolff-Parkinson-White Syndrome.

AF with Pre-Excitation (WPW Syndrome)

• Risk Assessment: Dangers of using AV nodal blockers (BB/CCB, digoxin, adenosine).
• Alternative Management: Utilization of procainamide or amiodarone for stable patients, synchronized electrical cardioversion for unstable patients.

Treatment Approaches for AF Types

• General Rapid AF:
  • First Line Agents: Metoprolol vs. Diltiazem.
  • Metoprolol Considerations: Dosing (5 mg every 10-15 minutes, max 15 mg), benefits in CAD and HF, limitations in asthma/COPD patients.
  • Diltiazem Advantages: Faster action, suitability in asthma/COPD, typical dosing (0.25 mg/kg initial, followed by 0.35 mg/kg if needed).
• Critically Ill Patients: Tailoring treatment to underlying pathology, avoiding typical AF pharmacologic treatments.

Systematic Evaluation of Tachycardia Causes (TACHIES Mnemonic)

• Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals (WPW), Embolus, Sepsis.
• Application of the mnemonic for a comprehensive approach to differential diagnosis.

Ultrasound in Diagnostic Assessment

• Application in Undiagnosed Tachycardia: Identifying EF, pericardial effusion, valvular pathology, and signs of pulmonary embolism.
• Fluid Status Evaluation: Use of ultrasound for assessing b-lines in lung scans.

Management of Chronic AF with HD Instability

• Assessment of Hemodynamic Impact: Effects of extreme tachycardia on cardiac output, preload and afterload considerations.
• Chronic vs. Paroxysmal AF: Differentiation in clinical presentation and treatment response.

Approaches in Complex AF Cases

• Addressing RVR of Unclear Etiology: Targeted therapies based on suspected underlying causes.
• Medication Strategies:
  • Amiodarone: Bolus and drip approach, slow AV nodal without significant impact on contractility.
  • Esmolol: Titration for heart rate control, short-acting nature allowing for rapid cessation if adverse effects are observed.

Comprehensive Patient Disposition

• Considerations: Hemodynamic stability, underlying cause, comorbidities, outpatient follow-up feasibility.
• Decision-Making Process: Balancing acute management with long-term treatment strategies.

Take Home Points

• Differentiation in AF with RVR Types: It’s essential to distinguish between primary AF with RVR, chronic AF with RVR related to other health issues, and new-onset AF (NOAF) with RVR in critically ill patients, as each type necessitates a unique approach to treatment.
• ACLS Guidelines for AF with RVR: The ACLS guidelines provide a treatment framework, particularly recommending immediate synchronized cardioversion for unstable patients. However, these guidelines may have limited effectiveness for chronic AF with RVR patients suffering from underlying critical illnesses.
• ECG Diagnosis in AF: Identifying AF on an ECG is crucial, with key indicators being an irregular rhythm without clear P waves and a ventricular rate exceeding 100 bpm. Accurate ECG interpretation guides effective treatment planning.
• Special Cases like WPW Syndrome: WPW syndrome and similar conditions require careful treatment consideration, as standard AF treatments can worsen these conditions. Alternatives like procainamide or amiodarone are often more appropriate.
• Patient-Centered Management of AF with RVR: Management should account for the patient’s overall health, underlying conditions, the chronicity of AF, and other comorbidities. Drugs like metoprolol and diltiazem offer benefits and risks, demanding personalized treatment plans.
• Pathophysiology in Critical AF Patients: Understanding the underlying pathophysiology in critically ill patients is vital. Tachycardia in these cases might be compensatory, necessitating an investigation into causes like myocarditis, dehydration, or GI bleeding.
• Systematic Evaluation with TACHIES Mnemonic: The mnemonic TACHIES (Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals [WPW], Embolus, Sepsis) aids in systematically assessing and addressing emergent tachycardia causes in critically ill patients.

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We discuss Electrical Storm (VT storm) and how to care for the very irritable heart.

Hosts:
Brian Gilberti, MD
Reed Colling, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Electrical_Storm.mp3 Download Leave a Comment Tags: Cardiology

Show Notes

Background/Overview of VT:

• Definition: What makes it a storm 
  • Three or more sustained episodes of VF, VT, or appropriate ICD shocks in a 24-hour period
• Pathophysiology: Understanding the origin and mechanism
  • Sympathetic drive/adrenergic surge
  • Underlying pathology: Sodium channelopathies, infiltrative disease like cardiac sarcoidosis, etc.
• RF’s / trigger / population (reversible cause in ~25% of patients)
  • MI
  • Electrolyte Derangements (emphasis on potassium and magnesium)
  • New/worsening heart failure
  • Catecholamine Surge
  • Drugs (stimulants, cocaine, amphetamines, etc)
  • QT Prolongation
  • Thyrotoxicosis

Clinical Presentation:

• Symptoms of VT: spectrum of symptoms – from palpitations to syncope to cardiac arrest
• Differentiating VT from other potential ER presentations.

Diagnostics in ER:

• Electrocardiogram (ECG): Recognizing VT patterns.
  • Monomorphic vs polymorphic (Torsades) may change management
  • Wide QRS
  • Fusion best
  • Capture beats
  • Concordance 
  • AV-dissociation
• Lab tests: Potassium, magnesium, troponins, TFTs, etc.

Acute Management in the ER:

• Hemodynamically stable vs. unstable V
  • Unstable = cardioversion
  • Sedation
    • Catecholamine surge should be considered 
    • No ideal agent 
    • Etomidate or propofol can be considered 
    • Ketamine may worsen irritability 
• Pharmacological treatments:
  • Amiodarone
    • Class III antiarrhythmic 
    • Most studied in VT storm 
    • First line
  • Beta Blockers
    • Propranolol
    • B1 and B2 activity 
• Non-pharmacological approaches:
  • Immediate synchronized cardioversion
  • IABP / ECMO considered for HD unstable patient
  • Cath lab if ischemic etiology suspected 
  • Stellate Ganglion Block

Take Home Points

• Definition: VT Storm is commonly defined as three or more sustained episodes of ventricular fibrillation, ventricular tachycardia, or appropriate ICD shocks within a 24-hour period.
• Varied Presentation: Patients may experience a range of symptoms from palpitations to severe hemodynamic instability.
• ECG and Diagnosis: Initial ECG may not show VT; continuous cardiac monitoring or device interrogation may be required for diagnosis.
• VT Identification: Look for wide QRS, rate over 100, fusion beats, capture beats, and AV dissociation to identify VT.
• Management in Hemodynamic Instability: Cardiovert if the patient shows signs of hemodynamic instability.
• Sedation Considerations: Be cautious with sedation, especially with ketamine, as it may worsen cardiac irritability in these already adrenergic state patients.
• Medication Choices: Typically, amiodarone and propranolol are used to manage VT Storm.
• Cardiology Involvement: Involve cardiology early on, as treatment may extend beyond medications.

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We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)

Hosts:
Brian Gilberti, MD
Jonathan Kobles, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3 Download 2 Comments Tags: Renal Colic

Show Notes

Introduction

1. Background

• • Physiology:
    • Normal range and the significance of deviations (>5.5 mEq/L)
  • Epidemiology:
    • Prevalence of hyperkalemia in the ER
    • ESRD missed HD → ECG, monitor

Causes / Risk Factors

• • Causes
    • Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia

• • High-Risk Medications:

• • • Antibiotics: Bactrim, antifungals

• • • Calcineurin inhibitors

• • • Beta-blockers

• • • ACE/ARB

• • • K+ Sparing diuretics

• • • NSAIDs

• • • Digoxin

• • • SUX – high risks in neuromuscular disease

• • Lab errors, hemolysis in samples
    • VBG vs Chem accuracy 
    • When to repeat a hemolyzed sample 
    • 2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).

Clinical Presentation / eval 

• Symptomatic vs. Asymptomatic:
  • “First symptom of hyperkalemia is death” 
  • If severe, ascending muscle weakness → paralysis 
    • Point at which patients experience symptoms depends on chronicity
      • >7 mEq/L if chronic and can be lower if acute
  • Hyperkalemia can be a cause of non-specific GI symptoms
• EKG Changes:
  • ECG findings may be the first marker the ER doc gets that something is wrong
  • Typical changes: 
    • Peaked T-waves, shortened QT
    • Lengthening of PR interval and QRS duration 
    • Bradycardia / Junctional rhythm
      • Hyperkalemia can produce bradycardia without other ECG findings
    • Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017)
  • Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG
    • Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998)
  • ECG changes are not linear, there is no exact association between K+ levels and ECG changes
  • ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs)
    • Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms
  • BRASH Syndrome
    • Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels. 
• Labs
  • Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice)
  • Consider evaluation for adrenal insufficiency
  • Waiting for labs may not be an option
    • Renal dysfunction + consistent ECG findings → prompt treatment before chem results
    • Realistically 2 hours to get back chemistry in most settings ≈ eternity

Management in the ER

• Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia

• A. Acute Management Strategies:
  • Cardiac protection with calcium
    • 1g over 5-10 mins
      • Lasts 30-60 mins, may have to redose 
      • Dose considerations if on digoxin 
      • AEs: Calciphylaxis and hypercalcemia
        • Fast pushes can result in hypotension, arrhythmia
    • Calcium chloride vs calcium gluconate
    • Caution in patients taking Digoxin
  • IVF choice – NS vs LR
    • Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL
  • Shifting potassium: 
    • insulin/glucose
      • 5 units vs 10 units 
        • 5 similar effect, less hypoglycemic episodes (LaRue 2017)
        • If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume 
      • Decrease but about 0.5-1.2 mEq/L
      • Effect starts 10-20 mins after administration and can last 4-6 hours
    • Albuterol
      • 10-20 mg over 10 mins (NB: higher dose than for asthma)
      • Peak effect at 90 mins
      • Decreases by 0.5 – 1.0 mEq/L alone
        • With insulin, ~1.2 mEq/L, additive effect 
    • Bicarbonate
      • Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue 
        • May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss
      • Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift.
  • Removal: 
    • Lokelma (Sodium Zirconium cyclosilicate)
      • Luckily residents have never had to use Kayexalate
      • Can start working in 1-2 hours of administration 
      • 0.37 mEq/L reduction at 4 hours after 10 g
      • Not a magic bullet in patients who need dialysis
    • Diuretics
      • No studies that demonstrate effectiveness in this ED setting
        • May be effective in patients with normal renal function
      • If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K
      • Nephron BOMB
        • Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex)
        • Thiazide (500-1000 mg IV chlorothiazide or 5-10 mg metolazone)
        • +/- Acetazolamide
        • +/- Fludrocortisone
          • May help stimulate the kidneys to secrete potassium
          • Primarily helpful in patients with mineralocorticoid deficiencies
    • Dialysis
      • Involve renal early because it takes a while to call in an HD nurse sometimes 
      • If no access and emergent HD is required → HD catheter placement
  • Strategies for suspected Brash syndrome
    • Epinephrine/Levo (if hypotensive/bradycardic)
    • Calcium gtt 
• Disposition/wrap up
  • Many factors at play here – patient preference, access, degree of hyperkalmia, identifiable / corrected cause 

Take Home points

• • Hyperkelamia causes can be put into three categories, pseudohyperkalemia, due to redistribution, and due to total body increase in potassium. Check out the show notes for a more complete list
  • Hyperkalemia can be difficult to pick up on before the labs come back because it can lurk without symptoms or even ECG changes
  • If a patient does have ECG changes, they may not follow that linear pattern that is traditionally taught and ECGs can be poorly sensitive. Now, if you do see changes, the ones that are more commonly associated with adverse events are QRS widening, junctional rhythm, and bradycardia
  • Treatment is a numbers game, calcium for cardiac stabilization can last just 30-60 minutes, insulin will be the fastest way to shift potassium back into cells, but be mindful that 10 units is associated with increased episodes of hypoglycemia whereas 5 units may have the same effect in reducing potassium. And albuterol is at a much higher dose than what is given for asthma 
  • Lokelma is now a pillar of treatment for removal of potassium. 
  • Diuretics with the goal of kiuresis may have a role in the oliguric patient, and increased doses along with other agents may buy time in patients with severe hyperK when HD is not readily available 
  • Involve renal early if you think that the patient will require HD

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We go over the essential and complex topic of vasopressors in the ED.

Hosts:
Brian Gilberti, MD
Catherine Jamin, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3 Download Leave a Comment Tags: Critical Care

Show Notes

Introduction

• Host: Brian Gilberti, MD
• Guest: Catherine Jamin, MD
  • Associate professor of Emergency Medicine at NYU Langone Health
  • Vice Chair of Operations
  • Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine
• Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED

What Are Vasopressors and When to Use Them

• Two primary mechanisms to increase blood pressure:
  1. Increasing systemic vascular resistance via vasoconstriction
  2. Increasing cardiac output via augmenting inotropy and chronotropy
• Indicators for vasopressor use:

• • MAP <65, systolic BP <90, or significant drop from baseline BP
  • Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate
  • Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients)

Commonly Used Vasopressors in the ED

• Norepinephrine
• Epinephrine
• Vasopressin
• Phenylephrine

Norepinephrine

• Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy)
• Starting Dose: 10 mcg/min, titrate to MAP >65
• Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min
• Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic)
• Pros: Can be infused peripherally via large bore IV

Vasopressin

• Mechanism: Activates V1a receptors causing vasoconstriction
• Dose: Fixed, non-titratable dose of 0.04 units/min
• Situational Preference: Second-line in septic shock
• Concerns: Potential for peripheral ischemia

Phenylephrine

• Mechanism: Stimulates alpha-1 receptors causing vasoconstriction
• Starting Dose: 100 mcg/min, titrate to MAP >65
• Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation
• Concerns: Increases afterload, can worsen low cardiac output states

Epinephrine

• Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors
• Starting Dose: 5-10 mcg/min, titrate to MAP >65
• Situational Preference: Anaphylactic shock, septic cardiomyopathy
• Limitations: Can induce tachycardia, may elevate lactate levels

Escalation Strategy in Refractory Shock

• Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine
• Consider POCUS, lactate, central venous saturation, and acid-base status

Peripheral Pressors

• Can safely be administered peripherally via large bore IVs in proximal upper extremity
• Sites: Cephalic or basilic veins
• Adverse Events: Low at 1.8% based on meta-analysis
• Actions in case of extravasation: Phentolamine injection, nitroglycerin paste

Push-Dose Pressors

• Primarily Phenylephrine (peri-intubation, during procedures)
• Also Epinephrine for peri-code situations
• Doses: Epi – 5-20 mcg every 2-5 min

Take-Home Points

• Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine.
• Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65
• Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock.
• Vasopressin is commonly the second we reach for in most of these scenarios
• Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock
• Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output
• The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access
• Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient

Additional References

• Importance of RUSH (Rapid Ultrasound in SHock) exam for diagnosis and treatment planning: https://emcrit.org/rush-exam/

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We discuss the diagnosis and management of septic arthritis in the pediatric population.

Hosts:
Brian Gilberti, MD
Ellen Duncan, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Joint_in_Children.mp3 Download 2 Comments Tags: Infectious Diseases, Pediatrics

Show Notes

• General

  • Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis

  • Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition.

  • Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint.

• Workup

  • Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain.

  • Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation.

  • Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach.

  • The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000.

1 criterion met = 3% probability of septic arthritis

2 criteria met = 40% probability of septic arthritis

3 criteria met = 93% probability of septic arthritis

4 criteria met = 99+% probability of septic arthritis

 

• If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available.

• Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies.

• Management

  • Empiric antibiotic therapy should target the most likely organisms and should not be delayed. Antibiotics may be narrowed once culture results are obtained.

  • The choice of antibiotics is dependent on the age group, with specific combinations suggested for neonates, children between 1 month and 4 years, and children aged 5 and older.

  • Cultures are only positive in 50-60% of cases. Synovial fluid PCR studies can help narrow antibiotic treatment.

• Take Home Points

  • Limp in the pediatric population can commonly be transient synovitis but we should always consider septic arthritis

  • Some clues in the history and physical that would point you towards septic arthritis include fever, refusal to bear weight, and limited range of motion on exam

  • We are going to have to get labs, including CBC, inflammatory markers, and preoperative labs, along with an XR and possibly an ultrasound

  • Kocher criteria is one tool that can help us determine if this is a patient that requires a joint tap.

  • Arthrocentesis is the gold standard for diagnosis, but antibiotics should be started promptly if the diagnosis is suspected.

  • The choice of antibiotics is dependent upon age group.

    • Neonates get vanc/cefepime, kids 1-4 yo get vanc / ceftriaxone

    • Older than 5 yo get vancomycin

      • Add ceftriaxone to them if patient has sickle cell disease, are immunocompromised, or Lyme or STI are suspected

  • Always cross check with institutional preferences / guidelines when choosing antibiotics

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A quick primer on hypocalcemia in the ED.

Hosts:
Joseph Offenbacher, MD
Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3 Download 4 Comments Tags: calcium, Critical Care, Endocrine

Show Notes

Swami’s CoreEM Post

Hypocalcemia Repletion:

• IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq
• For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours
•  For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve

References:

• Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298.
• ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209.
• Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis
• Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166.
• Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53.
• Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/
• Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163.

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How and when to reverse anticoagulation in the bleeding EM patient.

Hosts:
Joe Offenbacher, MD
Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3 Download 3 Comments Tags: Anticoagulation, Critical Care, Resuscitation

Show Notes

Coagulation Cascade:

 

Algorithm for Anticoagulated Bleeding Patient in the ED:

 

 

Indications for Anticoagulation Reversal:

 

References: 

1. Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001
2. Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008.
3. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
4. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
5. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643
6. Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317.

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