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Core EM - Emergency Medicine Podcast

192 Episodes

9 minutes | Apr 29, 2022
Podcast 186.0: Hypocalcemia
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 Leave a Comment Tags: calcium, Critical Care, Endocrine Show Notes
21 minutes | Feb 11, 2022
Podcast 185.0: Anticoagulation Reversal
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 Leave a Comment Tags: Anticoagulation, Critical Care, Resuscitation Show Notes Coagulation Cascade:   Algorithm for Anticoagulated Bleeding Patient in the ED:  
9 minutes | Dec 9, 2021
Episode 184.0 Ludwig’s Angina
A primer on this airway/ ID/ ENT emergency. Hosts: Joe Offenbacher MD, A Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3 Download One Comment Tags: Airway, ENT, Infectious Diseases Show Notes References: Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327. Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074. Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254. http://www.emdocs.net/ludwigs-angina-2/ Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306. Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506. Read More
13 minutes | Oct 29, 2021
Episode 183.0 Pneumothorax
A quick overview of pneumothorax for the EM physician: the what, why, diagnosis, and treatment. Hosts: Joe Offenbacher, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax_CoreEM_podcast.mp3 Download One Comment Tags: #pneumothorax #FOAMed Show Notes Shownotes: CoreEM Pulmonary Ultrasound Post
8 minutes | Sep 1, 2021
Episode 182.0 – Wellens
An interesting back story on this must-not-miss EKG finding in the ED! Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/CoreEM_Wellens.mp3 Download One Comment Tags: #FOAMed, #wellens, Cardiology, EKG, STEMI Show Notes Hosts: Joe Offenbacher MD, Audrey Bree Tse MD EKG Findings in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Table 1 in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. REFERENCES: de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Lee, M., & Chen, C. (2015). Myocardial Bridging: An Up-to-Date Review. Journal of Invasive Cardiology, 27(11), 521–528.  https://lifeinthefastlane.com/ecg-library/wellens-syndrome/ Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14;2017:bcr2017222835. doi: 10.1136/bcr-2017-222835. PMID: 29246935; PMCID: PMC5753703. Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638–643. https://doi.org/10.1053/ajem.2002.34800 Tandy, TK; Bottomy DP; Lewis JG (March 1999). “Wellens’ syndrome”. Annals of Emergency Medicine. 33 (3): 347–351. PMID 10036351. doi:10.1016/S0196-0644(99)70373-2. (via Wikipedia) Read More
20 minutes | Mar 4, 2021
Episode 181.0: Subarachnoid Hemorrhage
We discuss EM presentation, diagnosis, and management of subarachnoid hemorrhage. Hosts: Mark Iscoe, MD Brian Gilberti, MD Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SAH.mp3 Download One Comment Tags: Critical Care, Neurology, Subarachnoid Hemorrhage Show Notes Non-contrast head CT showing SAH (Case courtesy of Dr. David Cuete, Radiopaedia.org, rID: 22770)   Hunt-Hess grade and mortality (from Lantigua et al. 2015.) Hunt-Hess grade Mortality (%) 1. Mild Headache 3.5 2. Severe headache or cranial nerve deficit 3.2 3. Confusion, lethargy, or lateralized weakness 9.4 4. Stupor 23.6 5. Coma 70.5   Ottawa Subarachnoid Hemorrhage Rule, and appropriate population for rule application (from Perry et al. 2017) Apply to patients who are: Alert ≥ 15 years old Have new, severe, atraumatic headache that reached maximum intensity within 1 hour of osnet Do not apply to patients who have: New neurologic deficits Previous diagnosis of intracranial aneurysm, SAH, or brain tumor History of similar headaches (≥ 3 episodes over ≥ 6 months) SAH cannot be ruled out if the patient meets any of the following criteria: Age ≥ 40 Symptom of neck pain or stiffness Witnessed loss of consciousness Onset during exertion “Thunderclap headache” (defined as instantly peaking pain) Limited neck flexion on examination (defined as inability to touch chin to chest or raise head 3 cm off the bed if supine)   ___________________________ Special Thanks To: Dr. Mark Iscoe, MD (Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue) ___________________________ References: Bellolio MF, Hess EP, Gilani WI, et al. External validation of the Ottawa subarachnoid hemorrhage clinical decision rule in patients with acute headache. Am J Emerg Med. 2015;33(2):244-9. Carstairs SD, Tanen DA, Duncan TD, et al. Computed tomographic angiography for the evaluation of aneurysmal subarachnoid hemorrhage. Acad Emerg Med. 2006;13(5):486-492. Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737. Czuczman AD, Thomas LE, Boulanger AB, et al. Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap. Acad Emerg Med. 2013;20(3):247-256. Dugas C, Jamal Z, Bollu PC. Xanthochromia. [Updated 2020 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526048/ Goldstein JN, Camargo CA, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. 2006;26(6):684-90. Kumar A, Niknam K, Lumba-brown A, et al. Practice Variation in the Diagnosis of Aneurysmal Subarachnoid Hemorrhage: A Survey of US and Canadian Emergency Medicine Physicians. Neurocrit Care. 2019. Lantigua H, Ortega-Gutierrez S, Schmidt JM, et al. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015;19:309. Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666. Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions. Stroke. 1996;27(9):1558-63. Meurer WJ, Walsh B, Vilke GM, Coyne CJ. Clinical guidelines for the emergency department evaluation of subarachnoid hemorrhage. J Emerg Med. 2016;50(4):696-701. Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008;51(6):707-713 Perry JJ, Stiell IG, Sivilotti MLA, et al. High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study. BMJ. 2010;341:c5204. Perry JJ, Stiell IG, Sivilotti MLA, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343(jul18 1):d4277-d4277. Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-55. Perry JJ, Sivilotti MLA, Sutherland J, et al. Validation of the Ottawa Subarachnoid Hemorrhage Rule in patients with acute headache. CMAJ. 2017;189(45):E1379-E1385. Vermeulen MJ, Schull MJ. Missed diagnosis of subarachnoid hemorrhage in the emergency department. Stroke. 2007;38(4):1216-21. Read More
20 minutes | Jan 12, 2021
Episode 180.0: Urine Tox Screens
We discuss the (F)utility(?) of ED Utox screens with our very own Dr. Phil DiSalvo. Hosts: Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Urine_Drug_Screen_final.mp3 Download Leave a Comment Tags: Toxicology Show Notes Special Thanks To: Dr. Philip DiSalvo, MD Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue New York City Poison Control Center   References: Christian MR, et al. Do rapid comprehensive urine drug screens change clinical management in children? Clin Toxicol (Phila). 2017;57:977-980. Grunbaum AM, Rainey PM (2019).
14 minutes | Jul 26, 2020
Episode 179.0 – Precipitous Breech Deliveries
EM management of the rare but potentially complicated precipitous vaginal breech delivery. Hosts: Audrey Bree Tse, MD Masashi Rotte, MD MPH https://media.blubrry.com/coreem/content.blubrry.com/coreem/Breesashi_Breech_CoreEM.mp3 Download One Comment Tags: Obstetrics, Precipitous Deliveries, Pregnancy Show Notes Frank Breech Presentation: Complete Breech Presentation: Incomplete Breech (“Footling”) Presentation:   Pinard Maneuver:   Mauriceau Maneuver: References: Cunningham FG et al.  Breech Presentation and Delivery.  Williams Obstetrics, 22nd ed. 2005. Desai S, Henderson SO. Labor and Delivery and Their Complications. Rosen’s Emergency Medicine, 8e. 2014. Chapter 181. Gabbe SG et al.  Obstetrics: Normal and Problem Pregnancies, 2nd e. 1991. p.479. Stitely ML, Gherman RB. Labor with abnormal presentation and position. Obstet Gynecol Clin North Am. 2005; 32: 165. VanRooyen MJ, Scott J.  Emergency Delivery.  Tintanelli’s Emergency Medicine, 7th e.  2011.  Chapter 105. http://www.emdocs.net/the-complicated-delivery-what-do-you-do/#:~:text=Deliveries%20that%20occur%20in%20the,in%20denial%20of%20their%20pregnancies. https://ranzcog.edu.au/womens-health/patient-information-resources/breech-presentation-at-the-end-of-your-pregnancy https://wikem.org/wiki/Breech_delivery Read More
5 minutes | Jun 30, 2020
Episode 178.0 – Graduation Speech by Dr. Goldfrank
The speech given by Dr. Goldfrank at the 2020 NYU / Bellevue Emergency Medicine Graduation Ceremony https://media.blubrry.com/coreem/content.blubrry.com/coreem/Goldfrank_Graduation_Speech_2020.mp3 Download Leave a Comment Tags: Graduation. Goldfrank Show Notes Graduation 2020 Lewis R. Goldfrank, MD June 17, 2020 WELCOME TO THE GRADUATES Congratulations to a wonderful group of physicians. It is a pleasure to recognize your great accomplishments in the presence of your friends, families, loved ones and the residents and faculty who have learned so much from and with you. I would first like to recognize those of you who are members of the Gold Humanism Honor Society. There are a remarkable number of awardees in our graduating class of 2020. CLASS OF 2020 Joe Bennett (R) Max Berger (R) Ashley Miller (R) Leigh Nesheiwat (S) Kristen Ng (R) Emily Unks (S) AND Arie Francis (R) Nisha Narayanan (S) FUTURE PGY-4 Elena Dimiceli (S) Kamini Doobay (S) Mark Iscoe (R) FUTURE PGY-3 Stasha O’Callaghan (S) Nicholus Warstadt (S) FUTURE PGY-1 Aaron Bola (S) Alison (Ali) Graebner (S) Aron Siegelson (S) Melissa Socarras (S) Sarah Spiegel (S) Thomas Sullivan (S) Christy Williams (S) GOLD HUMANISM CORE VALUES Integrity, Excellence, Compassion, Altruism, Respect, Empathy, Service These are the values you want as a doctor for yourself or a loved one, to have outstanding listening skills with patients to be at your side during a medical emergency, to have exceptional interest in service to the community,
14 minutes | Feb 17, 2020
Episode 177.0 – Hemoptysis
An overview and management tips of hemoptysis in the ED. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hemoptysis.mp3 Download One Comment Tags: Critical Care, Pulmonary Show Notes OVERVIEW: Definition: expectoration/ coughing of blood originating from tracheobronchial tree Sources: Bronchial arteries (90%): under systemic circulatory pressure to supply supporting structures of the lung → heavier bleeding Pulmonary arteries (5%): under low pressure to supply alveoli → milder bleeding Nonbronchial arteries (5%): intercostal arteries, coronary arteries, thoracic/ upper/ inferior phrenic arteries Quantification: Mild: <20mL/ 24h Massive defined anywhere from >300mL-1L/ 24hr Mortality: 38% for massive (>500mL/ 24hr) vs 4.5% for nonmassive Etiology (in adults): Infectious (most common): Bronchitis PNA (necrotizing, lung abscess) TB Viral Fungal Parasitic Malignancy: Primary lung cancer vs metastatic disease Pulmonary: Bronchiectasis COPD PE/ infarction Bronchopleural fistula Sarcoidosis Cardiac: Mitral stenosis Tricuspid endocarditis CHF Rheumatological: Goodpasture Syndrome SLE Vasculitis (Wegener’s, HSP, Behcet) Amyloidosis Hematological: Coagulopathy/ thrombocytopenia/ platelet dysfunction DIC Vascular: Pulmonary HTN AA Pulmonary artery aneurysm Aortobronchial fistula Pulmonary angiodysplasia Toxins: Anticoagulation/ aspirin/ antiplatelets Penicillamine, amiodarone Crack lung Organic solvents Trauma: Tracheobronchial rupture Pulmonary contusion Other: bronchoscopy/ lung biopsy Pulmonary artery or central venous catheterization Foreign body aspiration Pulmonary endometriosis (catamenial hemoptysis) Idiopathic (up to 25% of cases) Pseudohemoptysis:  Sinusitis Epistaxis Rhinorrhea Pharyngitis URI Aspiration GIB WORKUP: HPI: CP, SOB B symptoms: fever, weight loss, chills, night sweats Lymphadenopathy Timeframe: acute vs chronic Prior lung/ renal/ cardiac disease Recreational drug/ cigarette/ chemical exposures travel/ infectious exposure Medications Any other sites of bleeding Precipitating factors Description of blood clots Patients are unable to accurately estimate degree of bleeding PE: Petechiae, edema, ecchymosis, ulcers, clubbing (chronic lung disease) Cardiopulmonary Sputum samples Labs: CBC w/ diff, BMP, LFTs, coags, T&S ABG UA Infectious workup if suspected: cultures, grain stains Imaging: CXR: 20% will be normal.  May see tumour, cavity, effusion, infiltrate, PTX.  Early pulmonary hemorrhage may present as infiltrate CT: only for stable patients!  May see bronchiectasis, cavitary lesions, acinar nodules, tumours CTA: bronchial arteries, aneurysms, PE ECHO: identify valvular abnormalities, signs of PE, aortic aneurysm Bronchoscopy: Not often performed in ED, but therapeutic & diagnostic Allows direct visualization of tumours, foreign bodies, granulomas, infiltration, as well as local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) MANAGEMENT: Goals: Control airway Protect healthy lung Identify and treat underlying cause Stabilize hemodynamics with volume resuscitation Provider precautions (respiratory & contact) ABCs, close monitoring Early airway management: massive hemoptysis, respiratory compromise, hypoxia, risk factors (elderly, AMS, coagulopathic) 2 x suction, preoxygenation, patient positioned upright, >8Fr ETT to facilitate suctioning/ bronch If bleeding side can be identified, consider “selective intubation” into nonbleeding lung to minimize further aspiration of blood and to provide ventilation Life threat = asphyxiation, not exsanguination.  ~Only 150cc anatomic dead space in major airways 2 x large bore IVs MTP prn vs volume resuscitation “Bad lung down” in lateral position: theoretical belief to minimize reflux of blood into normal lung Correct coagulopathy Consider nebulized TXA for nonmassive hemoptysis (500mg w/ NS per neb) Double-blind, randomized controlled trial in 2018 Nebulized TXA (500mg TID) vs placebo (normal saline) in hemodynamically stable adult patients admitted with mild hemoptysis (<200 mL/ 24hr) and no respiratory instability Additional exclusion criteria included those with renal failure, hepatic failure, or coagulopathy Assessed mortality and hemoptysis recurrence rate at 30 days and 1 year 25 patients randomized to receive TXA nebs, 22 randomized to receive normal saline nebs Results: Resolution of hemoptysis within 5 days of admission was significantly higher in TXA-treated patients than placebo patients (96% vs 50%; P < 0.0005) Mean hospital length of stay was shorter for TXA group (5.7 +- 2.5 days vs 7.8 +- 4.6 days; P = 0.046) Fewer patients in TXA group required invasive procedures to control bleeding vs placebo group (0% vs 18.2%; P = 0.041) No side effects were noticed in either group Antibiotics if infectious Bronchoscopy: local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) Rigid bronch for unstable patients to evacuate clots vs fiberoptic bronch for stable patients Bronchial artery embolization (call IR early!) May require lobectomy or pneumonectomy (consult thoracic surgery) DISPOSITION: Low threshold for higher level of care: only mild, hemodynamically stable hemoptysis on floor Discharge: only if certain regarding etiology in healthy, hemodynamically stable patients with scant, resolved hemoptysis, no coagulopathy, and reassuring workup Ensure patients have reliable follow up and avoid smoking. Strict return precautions!   REFERENCES: Kiraly A, Pang P, Cheema N.  Hemoptysis.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  5th Edition.  Philadelphia, PA: Wolters Kluwer; 2015; 504-505. Nickson, C.  Haemoptysis. Life in the Fastlane.  [litfl.com/haemoptysis/]. Updated April 9, 2019.  Retrieved February 10, 2020. Wand O, Guber E, Guber A, Schochet GE, Israeli-Shani L, Shitrit D.  Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial.  Chest. December 2018; 154(6): 1379-1384. Young WF.  Hemoptysis.  In: Cline, David,eds. Tintinalli’s Emergency Medicine Manual. 7th Edition.  New York : McGraw-Hill Medical; 2011; 473-476. Read More
10 minutes | Jan 27, 2020
Episode 176.0 – Pneumonia Updates
We go over the recent updates in the workup and management of pneumonia. Hosts: Brian Gilberti, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumonia_Updates.mp3 Download Leave a Comment Tags: Infectious Diseases, Pulmonary Show Notes 2007 Infectious Diseases Society of America/American Thoracic Society Criteria for Defining Severe Community-acquired Pneumonia Validated definition includes either one major criterion or three or more minor criteria Minor criteria Respiratory rate > 30 breaths/min PaO2/FIO2 ratio<250 Multilobar infiltrates Confusion/disorientation Uremia (blood urea nitrogen level > 20 mg/dl) Leukopenia* (white blood cell count , 4,000 cells/ml) Thrombocytopenia (platelet count , 100,000/ml) Hypothermia (core temperature , 368 C) Hypotension requiring aggressive fluid resuscitation Major criteria Septic shock with need for vasopressors Respiratory failure requiring mechanical ventilation A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More
15 minutes | Jan 13, 2020
Episode 175.0 – Posterior Circulation Stroke
Diagnosing and managing one of our critical diagnoses - posterior stroke. Hosts: Mukul Ramakrishnan, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/final_posterior_stroke_podcast_post_edit.mp3 Download One Comment Tags: Neurology, Posterior Stroke Show Notes See Dr. Newman-Toker demonstrate the HINTS exam here Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;40(11):3504-10   Read More
22 minutes | Dec 16, 2019
Episode 174.0 – Homelessness
We discuss one of the most complex problems we face – Homelessness Hosts: Kelly Doran, MD Audrey Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Homelessness.mp3 Download One Comment Tags: Social Emergency Medicine Show Notes Special Thanks To: Dr. Kelly Doran, MD MHS Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue ___________________________ References: Doran, K.M.  Commentary: How Can Emergency Departments Help End Homelessness?  A Challenge to Social Emergency Medicine. Ann Emerg Med. 2019;74:S41-S44. Doran, K.M., Raven, M.C. Homelessness and Emergency Medicine: Where Do We Go From Here? Acad Emerg Med. 2018;25:598-600. Salhi, B.A., et al. Homelessness and Emergency Medicine: A Review of the Literature. Acad Emerg Med. 2018;25:577-93. U.S. Department of Housing and Urban Development, Annual Homeless Assessment Report to Congress. Available at: https://www.hudexchange.info/resource/5783/2018-ahar-part-1-pit-estimates-of-homelessness-in-the-us/ U.S. Interagency Council on Homelessness. Home, Together Federal Strategic Plan to Prevent and End Homelessness. https://www.usich.gov/resources/uploads/asset_library/Home-Together-Federal-Strategic-Plan-to-Prevent-and-End-Homelessness.pdf Read More
12 minutes | Nov 25, 2019
Episode 173.0 – Blunt Neck Trauma
We go into one of the more complex injuries – blunt neck trauma. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Blunt_Neck_Injuries.mp3 Download One Comment Tags: Trauma Show Notes Overview Blunt neck trauma comprises 5% of all neck trauma Mortality due to loss of airway more so than hemorrhage Mechanism MVCs with cervical hyperextension, flexion, rotation during rapid deceleration, direct impact   Strangulation: hanging, choking, clothesline injury (see section on strangulation in this chapter) Direct blows: assault, sports, falls Initial Management/Primary Survey Airway Evaluate for airway distress (stridor, hoarseness, dysphonia, dyspnea) or impending airway compromise Early aggressive airway control: low threshold for intubation if unconscious patient, evidence of airway compromise including voice change, dyspnea, neurological changes, or pulmonary edema Assume a difficult airway  Breathing Supplemental oxygen Assess for bilateral breath sounds  Can use bedside US to evaluate for pneumothorax or hemothorax Circulation Assess for open wounds, bleeding, hemorrhage  IV access Disability Maintain C-spine immobilization  Calculate GCS Look for seatbelt sign Secondary Survey Evaluate for specific signs of vascular, laryngotracheal, pharyngoesophageal, and cervical spinal injuries with inspection, palpation, and auscultation Perform extremely thorough exam to evaluate for any concomitant injuries (e.g. stab wounds, gunshot wounds, intoxications/ ingestions, etc.) Types of Injuries Vascular injury Overview Carotid arteries (internal, external, common carotid) and vertebral arteries injured Mortality rate ~60% for symptomatic blunt cerebral vascular injury Mechanism Hyperextension and lateral rotation of the neck, direct blunt force, strangulation, seat belt injuries, and chiropractic manipulation Morbidity due to intimal dissections, thromboses, pseudoaneurysms, fistulas, and transections Clinical Features Most patients are asymptomatic and do not develop focal neurological deficits for days if Horner’s syndrome, suspect disruption of thoracic sympathetic chain (wraps around carotid artery) specific screening criteria are used to detect blunt cerebrovascular injury in asymptomatic patients (see below) Tintinalli 2016 Diagnostic Testing Gold standard for blunt cerebral vascular injury = MDCTA (multidetector four-vessel CT angiography) <80% sensitive but 97% specific Also images aerodigestive tracts and C-spine (unlike angiography) Followed by Digital Subtraction Angiography (DSA) for positive results or high suspicion  Angiography is invasive, expensive, resource-intensive, and carries a high contrast load Management Antithrombotics vs. interventional repair based on BCVI grading system Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology All patients with blunt cerebral vascular injury will require admission Tintinalli 2018 Pharyngoesophageal injury   Overview Rare in blunt neck trauma Includes hematomas and perforations of both pharynx and esophagus Mechanism Sudden acceleration or deceleration with hyperextension of the neck Esophagus is thus forced against the spine Clinical Features Dysphagia, odynophagia, hematemesis, spitting up blood Tenderness to palpation SC emphysema Neurological deficits (delayed presentation) Infectious symptoms (delayed presentation) Diagnostic Testing Esophagography with water-soluble contrast (e.g. Gastrograffin) If negative contrast esophagography, obtain flexible endoscopy (most sensitive) Combination of contrast esophagography + esophagoscopy has sensitivity close to 100% Swallow studies with water-soluble agent MDCTA Plain films of neck and chest  Findings such as pneumomediastinum, hydrothorax, or retropharyngeal air may suggest perforation but are not sensitive Management All pharyngoesophageal injuries receive IV antibiotics with anaerobic coverage Parenteral/ enteral nutrition NGT should only be placed under endoscopic guidance to avoid further injury Medical management vs. surgical repair depending on extent of injury Surgical repair for esophageal perforations or pharyngeal perforations >2cm Involve consultants early: trauma surgery, vascular surgery, otolaryngology, gastroenterology All patients with blunt cerebral vascular injury will require admission Laryngotracheal injury   Overview Occurs in >0.5% of blunt neck trauma Includes hyoid fractures, thyroid/ cricoid cartilage damage, cricotracheal separation, vocal cord disruption, tracheal hematoma or transection Mechanism Assault, clothesline injuries, direct blunt force from MVCs compressing the larynx between a fixed object and the spine Clinical Features Patients are often asymptomatic at first and then develop airway edema and/or hematoma resulting in airway obstruction Children are at higher risk for airway compromise due to less cartilage calcifications Diagnostic Testing Flexible fiberoptic laryngoscopy (FFL) to assess airway patency and extent of intraluminal injury MDCTA Obtain 1-mm cuts of larynx and perform multiplanar reconstructions  Consider POCUS to detect laryngotracheal separation Plain films of neck and chest Poor sensitivity for penetrating neck trauma injuries Can show extraluminal air, fracture or disruption of cartilaginous (e.g. larynx) structures  Management When securing airway, use an ETT that is one size smaller due to likelihood of airway edema Conservative management (IV antibiotics, steroids, observation) vs. surgical repair Grades III, IV, and V laryngotracheal injuries as defined by Schaefer and Brown’s classification system require OR Tintinalli 2018 Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology, otolaryngology  Cervical spine/ spinal cord injury   See chapter for spinal trauma Disposition Admit symptomatic patients to monitored setting Given delayed symptoms, consider monitoring patients who are asymptomatic on arrival Serial exams for worsening dyspnea, dysphonia, stridor, drooling, bruits, focal neuro deficits Only discharge after ruling out airway threat, neurological deficit, vascular injury, or suicidal/ homicidal ideation Monitor asymptomatic patients on home anticoagulation in ED for at least 6 hours from trauma to rule out delayed neck hematoma Social work and/or psychiatry for patients in whom you suspect suicide risk or domestric violence, look for other signs of self harm Take Home Points Aggressive early airway management for unconscious patient, evidence of airway compromise including voice change, dyspnea, neurological changes, or pulmonary edema Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology, otolaryngology  Victims of blunt cerebral vascular injury may present completely asymptomatic but develop delayed neurological symptoms; close observation and monitoring is recommended especially for patients on home anticoagulation Remember to evaluate for concomitant injuries Psychiatric evaluation for all attempted suicides References Bromberg, William. et al. Blunt Cerebrovascular Injury Practice Management Guidelines: The Eastern Association for the Surgery of Trauma. J Trauma. 68 (2): 471-7, Feb 2010.  Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540–545; discussion 545–546. Joshua AA.  Neck Trauma, Blunt, Anterior.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 5th Edition. Philadelphia, PA: Wolters Kluwer; 2015; 738-739. Tintinalli, J., Stapczynski, J. Stephan, editor, Ma, O. John, editor, Yealy, Donald M., editor, Meckler, Garth D., editor, & Cline, David, editor. (2018). Tintinalli’s emergency medicine : A comprehensive study guide (9th ed.). Walls, R., Hockberger, Robert S., editor, & Gausche-Hill, Marianne, editor. (2018). Rosen’s emergency medicine : Concepts and clinical practice (Ninth ed.). Advanced trauma life support. (2018). 10th ed. Chicago, IL: American College of Surgeons. Special thanks to Sana Maheshwari, MD  NYU Bellevue Emergency Medicine Residency PGY3   Read More
11 minutes | Nov 4, 2019
Episode 172.0 – Ankle Sprains
We dissect one of the most common injuries we see in the ER -- ankle sprains Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ankle_Sprains.mp3 Download 3 Comments Tags: Orthopedics Show Notes Background Among most common injuries evaluated in ED A sprain is an injury to 1 or more ligaments about the ankle joint Highest rate among teenagers and young adults Higher incidence among women than men Almost a half are sustained during sports Greatest risk factor is a history of prior ankle sprain Anatomy Bone: Distal tibia and fibula over the talus → constitutes the ankle mortise Aside from malleoli, ligament complexes hold joint together Medial deltoid ligament Lateral ligament complex Anterior talofibular ligament Most commonly injured Weakest 85% of all ankle sprains  Posterior talofibular ligament Calcaneofibular ligament Syndesmosis Mechanism of Injury Lateral ankle sprains  Most common among athletes ATFL most commonly injured Combined with CFL in 20% of injuries 2/2 inversion injuries Medial ankle sprains Less common than lateral because ligaments stronger and mechanism less frequent More likely to suffer avulsion fracture of medial malleolus than injure medial ligament 2/2 eversion +/- forced external rotation Typically landing on pronated foot -> external rotation High Ankle sprains Syndesmotic injury More common in collision sports (football, soccer, etc) Grade I Mild Stretch without “macroscopic” tearing Minimal swelling / tenderness No instability No disability associated with injury     Grade II Moderate Partial tear of ligament Moderate swelling / tenderness Some instability and loss of ROM Difficulty ambulating / bearing weight     Grade III Severe Complete rupture of ligaments Extensive swelling / ecchymosis / tenderness Mechanical instability on exam Inability to bear weight Examination     Beyond visual inspection for swelling, ecchymoses, abrasions, or lacerations Palpation  Pain when palpating ligament is poorly specific but may indicate injury to structure Check sites for Ottawa ankle rules to evaluate if there may be an associated fracture with injury Posterior edge or tip of lateral malleolus (6 cm) Posterior edger or tip of medial malleolus (6 cm) Base of fifth metatarsal Navicular bone Acute ATFL rupture / Grade III Sprain 90% chance of this injury if hematoma and localized tenderness with palpation present on exam over this ligament  Anterior drawer test Assess for anterior subluxation of talus from the tibia Ankle in relaxed position, distal extremity is stabilized with one hand while the other cups the heel to apply anterior force Compare to contralateral side Difficult to determine if there is an acute rupture at this point and may be more easily diagnosed in subacute phase (4-5 days after injury) Ability to perform exam adequately limited by pain, swelling and potential muscle spasm Talar tilt test If applying inversion force to ankle and there is excessive mobility → calcaneofibular ligament Thompson test Can be performed if there is concern for concomitant Achilles tendon injury  Do not miss a Maisonneuve fracture by palpating proximally about the fibular ahead as forces may be transmitted through the syndesmosis  Squeeze test – pressure just proximal to ankle If elicits pain → concern for syndesmotic injury Diagnostics     X-rays indicated if unable to rule out using Ottawa Ankle Rules Sn (Up to 99.6) (one of the best validated tools we use in the ER) May have trouble applying rule if there is question of patients ability to sense pain (diabetic neuropathy), in which case obtain radiographs Treatments     RICE Crutch train so they can be weight bearing a tolerated Ideally initiate within first 24 hours of injury Ice 15-20 minutes q2-3h over the first 48 hours or until swelling improves     NSAIDs Topical and PO are better than placebo  We do not know if PO is superior to topical NSAIDs     Early mobilization / Functional Rehab (sample patient instructions here) Work to restore range of motion, strength, proprioception For Grade I and II, can begin as soon as the patient can tolerate and ideally within 1 week of the injury Patients return to work sooner, decreased chronic instability, less recurrent injuries Dorsiflexion, plantarflexion, and perform foot circles as well as toe curls, inversion and eversion as tolerated Proprioception Balancing on wobble board Continue exercises until patient is able to return to activities at full capacity, without pain Immobilization High re-injury rates and important to protect against this Grade I No immobilization required +/- Ace wrap Grade II Aircast brace Ensure patient understands that they should still partake in rehabilitation exercises Grade III Data conflicts RCT, multicenter study comparing aircast brace, compression bandage, Bledsoe immobilization boot and below-knee cast for 10 days Ankle function at 3 months Cast group had most improvement No difference at 9 months in function or complications May be institution-dependent and a cast can be offered initially Prognosis Acute inflammation → reduction in swelling → development of new tissue → strengthening of tissue  Return of basic function, though limited, occurs over 4-6 weeks depending on severity of sprain Try to limit strain put on joint (no heavy lifting, walking on uneven surfaces, try to limit standing while at work) Follow up: If pain or instability does not improve over 4-6 weeks Grade III sprains Medial ankle sprains (may have underlying fracture that was undetected in ED on XR) Syndesmosis injuries (protracted recovery course) Injuries associated with fractures or dislocation / subluxation   Read More
16 minutes | Oct 21, 2019
Episode 171.0 – Vaping Associated Lung Injury
An overview of Vaping Associated Lung Injury (VALI) Hosts: Audrey Bree Tse, MD Larissa Laskowski, DO Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vaping_Associated_Lung_Injury.mp3 Download 2 Comments Tags: Pulmonary, Toxicology Show Notes Why this matters As of Oct 15, vaping has been associated with acute lung injury in over 1400 people 33 deaths have been confirmed in 24 states 70+% of those with VALI are young men A large number of patients are requiring ICU/ intubation/ ECMO 4 main ingredients in solvent +/- Flavor additives +/- Nicotine or THC (Tetrahydrocannabinol) Propylene Glycol (PG) Vegetable Glycerin (VG) CDC definition of VALI (Vaping Associated Lung Injury) Using an e-cigarette (“vaping”) or dabbing* in 90 days prior to symptom onset AND Pulmonary infiltrate, such as opacities, on plain film chest radiograph or ground-glass opacities on chest CT AND Absence of pulmonary infection on initial work-up.  No evidence in the medical record of alternative plausible diagnoses (e.g., cardiac, rheumatologic, or neoplastic process). *Dabbing allows the user to ingest a high concentration of THC.  Butane Hash Oil (BHO), an oil or wax-like substance extracted from the marijuana plant, is placed on a “nail” attached to a specialized glass bong called a “rig.” A blow torch is used to heat the wax, which produces a vapor that can then be inhaled to supposedly produce an instantaneous effect. Pathophysiology At present, no single compound or ingredient has emerged as the cause, and there may be more than one cause The only common thread among the cases is that ALL patients reported using e-cig or vaping products Leading potential toxins: Vaping products containing THC concentrates: most cases are linked to THC concentrates that were either purchased on the street or from other informal sources (meaning not from a dispensary) Vitamin E acetate: nutritional supplement safe when ingested or applied to the skin (but likely not when inhaled) has been found in nearly all product samples of NY state cases of suspected VALI vitamin E acetate is NOT an approved additive at least by NYS Medical Marijuana program Other potential toxins: IT CANNOT BE UNDERSTATED that a small percentage of persons w/ VALI have reported exclusive use of nicotine-containing vape products, such as JUUL; as such, we must consider the potential toxicity of standard e-liquid or vape juice Flavor additives, that exists as chemical aldehydes: irritating and potentially damaging to lung tissue PG/VG: shown not only to break down to formaldehyde which is a known carcinogen, but also to produce lipoid pneumonia in rat lungs Some devices are easily manipulated to increase the capacity to produce vapor; increasing these settings may impact heating temperature, metabolic breakdown, and release of microscopic metal particles Lungs are multifunctional, including serving as an immune organ: lungs cleave proteins of all of the bacteria, viruses and other pathogens we are exposed to and inhale daily human studies on those that are chronic e-cig users or vapers have revealed that these products are shifting the balance of proteases and antiproteases in our lungs such that the proteases are destroying native lung tissue similar to how traditional cigarettes cause COPD Many potential reactions: NEJM article in references: details four radiographic phenotypes essentially reflecting different pathologic changes Long-term Effects Long term effects are unknown (some pts have required home oxygen on discharge) Risk for recurrence or relapse, especially if repeat exposure Presentation 95% of pts have had pulmonary sxs (cough, cp, dyspnea) 77% of pts have had GI sxs (abd pain, n/v/d) 85% of pts w/ constitutional sxs (f/c, weight loss) 57% w/ hypoxia (O2 < 95%) Unfortunately auscultation has been unreliable and poorly sensitive Workup There is no specific test or marker for dx, so VALI is still considered a dx of exclusion Labs: CBC ESR/CRP (93% w/ elevated ESR) LFTs (50% w/ transaminitis) ABG: hypoxia Imaging: CXR: typically shows bilateral infiltrates, although not always and there have even been some cases w/ unremarkable chest XR (so high degree of clinical suspicion in any person p/w hypoxia) CT: ground glass opacities, typically bilaterally  Management Dispo: 96% of cases required hospitalization Any pt w/ hypoxia, respiratory distress, or comorbidities Outpatient only if: no hypoxia or respiratory distress, reliable followup within 48h and good social support (keep in mind that some patients w/ mild symptoms of first presentation deteriorated rapidly within 48h) Empiric treatments for pneumonia inc abx, antivirals Steroids (methylpred 60mg q6h, based on how index cases in Illinois were managed) Case reports have documented improvement Mechanism: blunting of inflammatory response Aggressive supportive care Special Thanks To: Dr. Larissa Laskowski, DO Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue New York City Poison Control Center References: Outbreak of Lung Injury Associated with E-Cigarette Use, or Vaping.  https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html Carlos WG, Crotty Alexander LE, Gross JE, Dela Cruz CS, Keller JM, Pasnick SP, Jamil S.  Vaping-associated Pulmonary Illness (VAPI). Public Health Information Series. Am J Respir Crit Care Med Vol. 200, 13-15, 2019.  www.atsjournals.org/doi/pdf/10.1164/rccm.2007P13 Henry TS, Kanne JP, Kilgerman SJ.  Images of Vaping-Associated Lung Disease — Correspondence.  N Engl J Med. 2019 Oct 10; 381;15.   Layden JE, Ghana I, Pray I, Kimball A, Layer M, Tenforde M, Navon L, Hoots B, Salvatore PP, Elderbrook M, Haupt T, Kanne J, Patel MT, Saathaff-Huber L, King BA, Schier JG, Mikosz CA, Meiman J.  Pulmonary Illness Related to E-Cigarette Use in Illinois and Wisconsin – Preliminary Report.  N Engl J Med. 2019 Sep 6. doi: 10.1056/NEJMoa1911614. [Epub ahead of print].  https://www.ncbi.nlm.nih.gov/pubmed/31491072?dopt=AbstractPlus Siegel DA, Jatlaoui TC, Koumans EH, et al. Update: Interim Guidance for Health Care Providers Evaluating and Caring for Patients with Suspected E-cigarette, or Vaping, Product Use Associated Lung Injury — United States, October 2019. MMWR Morb Mortal Wkly Rep 2019;68:919–927. DOI: http://dx.doi.org/10.15585/mmwr.mm6841e3external icon. https://www.health.ny.gov/press/releases/2019/2019-09-05_vaping.htm Read More
11 minutes | Sep 23, 2019
Episode 170.0 – Septic Arthritis
An overview of septic arthritis. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Arthritis.mp3 Download One Comment Tags: Infectious Diseases, Orthopedics Show Notes Episode Produced by Audrey Bree Tse, MD Background Bacteria enters the joint by hematogenous spread due to absence of basement membrane in synovial space from invasive procedures, contiguous infection (e.g. osteomyelitis, cellulitis), or direct inoculation (e.g. plant thorns, nails) WBCs migrate into joint → acute inflammatory process → synovial hyperplasia, prevents new cartilage from forming, pressure necrosis on surrounding joint, purulent effusion Why do we care?  irreversible loss of function in up to 10% & mortality rate as high as 11% Cartilage destruction can occur in a matter of hours Complications include bacteremia, sepsis, and endocarditis Etiology Risk factors: extremes of age, RA, DJD, IVDA, endocarditis, GC, immunosuppression, trauma, or prosthesis Organisms:  Staph: staph aureus (most common), MRSA, Staph epidermis N gonorrhea: young healthy sexually active adults Strep: group A & B GNRs: IVDA, diabetics, elderly Salmonella: sickle cell disease Cutibacterium acnes: prosthetic shoulder infection Consider mycobacterial & fungal in more indolent courses Presentation Typically a single, warm, erythematous, tender joint (#1: knee (50% of cases) → hip, shoulder, ankle) *Any joint can be involved! IVDA can involve sacroiliac, costochondral, & sternoclavicular joints  Classic teaching: very painful with ROM, but this is not always present! Joint usually held in position of maximum joint volume Prosthetic joints may have less pain than expected for a septic joint given changed anatomy and disrupted nerve endings In 10-20% of cases, can see polyarticular involvement GC typically monoarticular but commonly polyarticular Often have fever & separate infection as well (only see fever in ~60% of cases) Diagnostics Arthrocentesis:  Gold standard  Tap joint even if acceptable ROM: septic joints can have normal motion so it does not exclude the diagnosis! Use ultrasound if possible Relative contraindications: overlying cellulitis (risk of seeding joint) or severe coagulopathies (weigh risk of creation or worsening of iatrogenic hemarthrosis) Keep in mind that a “dry tap” may occur due to incorrect needle placement, absent/ minimal joint effusion, ort mechanical obstruction Note: talk to ortho colleagues if prosthesis present prior to performing arthrocentesis  Ortho team may want to perform the arthrocentesis themselves because scar tissue formation and altered anatomic relationships make the procedure more challenging Usually want to perform washout in OR plus/ minus antibiotic spacer Send fluid for protein, glucose, cell count with differential, gram stain, culture, and crystals Often see decreased glucose and elevated protein The presence of crystals does not rule out septic arthritis No clear number of synovial WBCs to define septic arthritis, but in general: >30 to 50K/ mm3 synovial WBCs with PMN predominance (>75%) seen in septic arthritis A 2011 meta-analysis suggests +LRs of 4.7 (95% CI = 2.5 to 8.5) and +LR of 13.2 (95% CI = 3.6 to 51.1) for a sWBC count of >50L × 109 or >100K, respectively Use the synovial WBC count plus the whole clinical picture to rule in or out the diagnosis of septic arthritis (do not use the synovial WBC in isolation) Different threshold for prosthetic joints: WBC > 1100 or >64% PMNs = septic arthritis Gram stains only identify causative organisms 1/3 of the time Culture negative arthrocentesis can be seen in cases where abx have been given prior to arthrocentesis, or in TB/ brucella/ nocardia/ other indolent organisms like fungi Labs: No studies have demonstrated an acceptable sensitivity or overall diagnostic accuracy of peripheral WBC count for SA, but usually see leukocytosis with left shift ESR and CRP are reasonably sensitive but there is no cutoff that significantly increases or decreases the pretest probability UA, urine cultures, blood cultures: send even if no fever Blood cultures are positive in 50-70% of nonGC SA If GC suspected, do GC NAAT from throat/ rectal/ urethral/ cervical discharge Imaging: XRs: effusion, baseline status of joint, contiguous osteomyelitis, fractures, foreign body US: effusion CT, MRI: not really used in ED Differential Viral arthritis RA gout/ pseudogout HIV associated arthritis Reactive arthritis Lyme Osteo Septic bursitis Trauma Treatment Septic arthritis is an orthopedic emergency! Needs IV abx + often washout of the joint Hold abx as much as possible prior to tap unless pt is unstable or tap cannot be performed easily Initiate empiric IV antibiotic therapy prior to definitive cultures based Transition to organism-specific antibiotic therapy once culture sensitivities result Start empiric abx based on gram stain if available (in non-=GC SA, grain stain is positive in 50% of cases), age group, & risk factors Empiric abx: Vancomycin 15mg/kg q12h (to cover MRSA) + cefepime 2gr IV q8h (to cover gram-negatives) If gram stain with GPC = Vancomycin 15mg/kg q12h If gram stain with GN diplococci = ceftriaxone 1gr IV q24h + Azithromycin 1gr q24h If gram stain with GN rods = cefepime 2gr IV q8h If penicillin allergy: ciprofloxacin 500mg q12h or aztreonam 2gr q8h No need to cover anaerobes unless human/dog/cat bite (then use Unasyn to cover eikenella, pastereulla, capnocytophaga, anaerobes, etc.) They usually need antibiotics for 2-6 weeks: 2 weeks for strep, up to 6 weeks if S aureus   Pain control: consider moderately flexed splinting Admit all patients with suspected septic arthritis until SA is ruled out, abx, monitoring, likely operative intervention Take-Home Points Patients may present with either a single affected joint or polyarticular; they may or may not have a fever Have a high index of suspicion for SA, and a low threshold to tap: pts do not necessarily present w/ “classic” findings and it is difficult to distinguish SA from crystal arthropathy ESR, CRP, serum WBC are not definitive diagnostic tools for septic arthritis There is no exact cutoff for synovial WBCs for diagnosis: use whole clinical picture & keep 50K in mind for native joints, and >1100 for prostheses Treat with empiric abx after tap then narrow accordingly, & admit all patients with septic arthritis Involve your ortho colleagues early especially for prosthesis References Carpenter CR, Schuur JD, Everett WW, et al.  Evidence-based diagnostics: Adult septic arthritis.  Acad Emerg Med.  2011;18:781-796. Jones D, Clements C.  Physical exam and bloodwork do not adequately differentiate infectious from inflammatory arthritis.  In: Mattu A, Chanmugam A, Swadron S, Woolridge D, Winters M.  Avoiding Common Errors in the Emergency Department. 2nd Edition.  Philadelphia, PA: Wolters Kluwer; 2017; 412-414.   Kazzi A, Zaghrini E.  Septic Arthritis.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  5th Edition.  Philadelphia, PA: Wolters Kluwer; 2015; 102-103. Osmon D, Berbari E, Berendt A, Lew D, Zimmerli W, Steckelberg J, Rao N, Hanssen A, Wilson W.   Diagnosis and Management of Prosthetic Joint Infection: Clinical Practice Guidelines by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 56, Issue 1, 1 January 2013, Pages e1–e25, https://doi.org/10.1093/cid/cis803 Mlynarek C, Sullivan A.  Arthrocentesis Tips.  In: Mattu A, Chanmugam A, Swadron S, Woolridge D, Winters M.  Avoiding Common Errors in the Emergency Department. 2nd Edition.  Philadelphia, PA: Wolters Kluwer; 2017; 684-686. Purcell D, Terry B, Sharp B.  Joint Arthrocentesis.  In: Purcell D, Chinai S, Allen B, Davenport M.  Emergency Orthopedics Handbook. 1st Edition. Cham, Switzerland: Springer; 2019; 87-104. Sheth U, Moore D.  Septic Arthritis — Adult.  OrthoBullets.  [https://www.orthobullets.com/trauma/1058/septic-arthritis–adult].  Updated 1/9/19.  Accessed 8/2/19.   A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine   A special thanks to our Orthopedics Editor: Daniel Purcell, MD Emergency Medicine NYU Langone Brooklyn   Read More
9 minutes | Aug 26, 2019
Episode 169.0 – Febrile Seizures
A look at the most common type of seizures in the young pediatric population. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Febrile_Seizures.mp3 Download Leave a Comment Tags: Pediatrics Show Notes Background The most common type of seizure in children under 5 years of age Occur in 2-5% of children In children with a fever, aged 6 months to 5 years of age, and without a CNS infection Risk Factors 4 times more likely to have a febrile seizure if parent had one Also increase in risk if siblings or nieces / nephews had one Common associated infections Human Herpesvirus 6 Human Herpesvirus 7 Influenza A & B Simple Febrile Seizure Generalized tonic-clonic activity lasting less than 15 minutes in a child 6 months to 5 years of age Complex Febrile Seizure Lasts longer than 15 minutes, occurs in a child outside of this age range, are focal, or that recur within a 24-hour period. Diagnostics / Workup Gather thorough history and perform thorough physical exam Most cases will not require labs, imaging or EEG If e/o meningitis, perform LP AAP suggests considering LP in: Children 6-12 months who are not immunized for H flu type B or strep pneumo Children who had been on antibiotics For complex seizures, clinician may have a lower threshold for obtaining labs Hyponatremia is more common in this group than in the general population. LPs are more commonly done by providers, but these are low yield with one study showing bacterial meningitis being diagnosed in just 0.9% (Kimia 2010), all of whom did not have a normal exam or negative cultures. Neuroimaging is also exceedingly low yield if the patient returns to baseline (Teng 2006) One study that showed that the duration of complex febrile seizure, being greater than 30 minutes, was associated with a higher incidence of bacterial meningitis. (Chin 2005) Of they have history and exam concerning for meningitis, they should get an LP If they look dehydrated or edematous, you would have more of a reason to get a chemistry Treatment Benzodiazepine if seizure lasted for >5 minutes, either IV or IN Supportive care Tylenol or motrin if febrile Fluids if signs of dehydration Antipyretics “around the clock” A majority of data show no benefit in preventing recurrence of seizure One study (Murata 2018) found that giving tylenol q6h at 10 mg/kg for the first 24 hours following the initial seizure decreased the rate of recurrence when compared to children who did not receive antipyretics. NNT here was 7 Questionable whether we can generalize these findings from a single ED in Japan. No role for antiepileptics Prognosis High rate of recurrence (~1/3) within 1 year of initial seizure Risk increases for Younger age at which they had initial seizure Lower temperature at which they had seizure If initial febrile seizure was prolonged, more likely that the next will be prolonged 1-2% develop epilepsy for simple febrile seizure, slightly above risk of general population 5-10% develop epilepsy for complex febrile seizure Follow up with PMD Generally, peds neuro follow up is not necessary References Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. 2005;90(1):66-9. Kimia A, Ben-Joseph EP, Rudloe T, Capraro A, Sarco D, Hummel D, et al. Yield of lumbar puncture among children who present with their first complex febrile seizure. Pediatrics. 2010;126(1):62-9. Murata S, Okasora K, Tanabe T, Ogino M, Yamazaki S, Oba C, et al. Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018;142(5). Patel N, Ram D, Swiderska N, Mewasingh LD, Newton RW, Offringa M. Febrile seizures. BMJ. 2015;351:h4240. Pavlidou E, Panteliadis C. Prognostic factors for subsequent epilepsy in children with febrile seizures. Epilepsia. 2013;54(12):2101-7. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide, 8th Edition. New York: McGraw-Hill Education. Subcommittee on Febrile S, American Academy of P. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-94. Teng D, Dayan P, Tyler S, Hauser WA, Chan S, Leary L, et al. Risk of intracranial pathologic conditions requiring emergency intervention after a first complex febrile seizure episode among children. Pediatrics. 2006;117(2):304-8. Warden CR, Zibulewsky J, Mace S, Gold C, Gausche-Hill M. Evaluation and management of febrile seizures in the out-of-hospital and emergency department settings. Ann Emerg Med. 2003;41(2):215-22. A special thanks to our editors: Michael A. Mojica, MD Director, Pediatric Emergency Medicine Fellowship Bellevue Hospital Center Christie M. Gutierrez, MD  Pediatric Emergency Medicine Fellow Columbia University Medical Center Morgan Stanley Children’s Hospital New York Presbyterian   Read More
15 minutes | Jul 30, 2019
Episode 168.0 – Lyme Disease
A review for the emergency physician of this common tick-borne illness. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Lyme_Disease.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Episode Produced by Audrey Bree Tse, MD Background Most common tick-born illness in North America Endemic in Northeast, Upper Midwest, northwest California 80% to 90% in summer months Pathophysiology Ixodes tick (deer tick) has a 3-stage life cycle (larvae, nymph, adult) & takes 1 blood meal per stage Deer tick feeds on an infected wild animal (infected with spirochete Borrelia burgodrferi) then bites humans On humans, they typically move until they encounter resistance (e.g. hairline, waistband, elastic, skin fold).  It takes 24-48 hrs for B. Burgdorferi to move from the tick to the host Pathogenesis: organism induced local inflammation, cytokine release, autoimmunity No person to person transmission Clinical Presentation Stage 1: Early Symptom onset few days to a month after tick bite Erythema migrans rash: bulls eye rash seen in more than 90% of patients with Lyme disease (Irregular expanding annular lesion(s)) Regional adenopathy, intermittent fevers, headache, myalgias, arthralgia, fatigue, malaise Stage 2: disseminated/ secondary Days to weeks after tick bite Intermittent fluctuating sx that eventually resolve Triad of aseptic meningitis, cranial neuritis, and radiculoneuritis: bell palsy most common Cardiac symptoms: tachycardia, bradycardia, AV block, myopericarditis Stage 3: tertiary/ late Symptoms occur >1 year after tick bite Acrodermatitis chronic atrophicans: Atrophic lesions on extensor surfaces of extremities (resembles scleroderma) Monoarthritis, oligoarthritis (knee > shoulder > elbow) GI: Hepatitis, RUQ pain Ocular: keratitis, uveitis, iritis, optic neuritis Neurological: Chronic axonal polyneuropathy or encephalopathy Chronic Lyme disease (versus well-accepted Lyme disease sequelae): Continuation of symptoms after antibiotics Current recommendation for management is supportive care only Pediatric considerations: More likely to be febrile than adults Facial palsy accompanied by aseptic meningitis in 1/3 Untreated kids can develop keratitis Excellent prognosis if appropriately treated History Travel, camping, woods, playing under leaves or in wood piles Living in endemic area (Northeastern area: Maine to Virginia; upper Midwestern: Wisconsin, Minnesota; Northwest California) Endemic in Northern Europe and Eastern Asia as well History of tick bite (- 30-50% of patients recall tick bite) Flu like illness in summer Rash: https://www.cdc.gov/lyme/signs_symptoms/rashes.html Joint complaints Cardiac complaints Neurologic complaints Careful search for tick Diagnosis Labs CBC (leukocytosis, anemia, thrombocytopenia) ESR: most common lab abnormality (>30 mm/hr) Chem 7 LFTs: commonly elevated especially GGT Cultures not typically indicated LP when meningeal signs (CSF: pleocytosis, elevated protein, CSF spirochete ABs).  LP function is more to rule out other etiologies of meningitis rather than diagnose Lyme meningitis given that lyme PCR and lyme Ab index are not very accurate. Serological Testing Serological testing is not always warranted because of the very high incidence of false positive results Serologies are not useful in acute phase (<30 days of infection) because they are negative; it takes several weeks to develop enough antibodies for either test below (ELISA or Western Blot) Acute Lyme is a clinical diagnosis and does not need laboratory testing, especially in endemic areas such as NY If pretest probability is high (symptoms consistent with Lyme + epidemiological background), say patients with CN palsy, meningitis, carditis, or migratory large joint arthritis, then serologies can be very helpful Do not test if patients in endemic areas with potential tick exposure present with EM — just treat with antibiotics Do not test if patients in endemic areas present with no history of tick exposure or only nonspecific symptoms Test if you have high suspicion of lyme without EM PCR is highly specific and sensitive but not available for routine use.  There are two tests you need to use together: 1) ELISA: this detects antibodies to lyme bacteria (borrelia burgdorferi)  in your blood, BUT it can’t distinguish between borrelia and similar bacteria (even sometimes normal flora that lives in you).  In addition, IgM response takes 1-2 weeks while IgG response takes 2-4 weeks. If ELISA is positive or equivocal, then you move onto the: 2) Western blot test: this looks for antibodies not to the whole organism, but to the basic building blocks of the lyme bacteria — the individual proteins, BUT many types of bacteria use the same building blocks. So the CDC says that the Western Blot test must detect IgG antibodies to 5 out of the 10 proteins. See figure 2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918152/ Two-tiered testing has sensitivity between 70-100% and specificity ~95% in late stages Interpretation of Lyme serologies should be done by an ID specialist because they can be confusing and can lead to wrong conclusions if unfamiliar with them NYC is an endemic region where 5% of the population can have a positive without symptoms! If somebody who HAD Lyme disease but successfully treated it with doxycycline tested themselves years later, they could still have the antibodies and therefore it would look like they still had Lyme disease (despite being cured) Positive serology or previous Lyme disease not ensure protective immunity Other tests: Arthrocentesis for acute arthritis: elevated cryoglobulin XRs: may show soft tissue, cartilaginous, osseous changes ECG Differential Diagnosis Tick-borne diseases: Rocky Mountain Spotted fever, tularemia, relapsing fever, Colorado tick fever, tick-bite paralysis, babesiosis, anaplasmosis, powassan virus Remember that doxycycline covers anaplasmosis and lyme but not babesiosis, which requires Atovaquone Rheumatic fever (usually presents with erythema marginatum rash, valvular involvement rather than heart block, TM joint arthritis) Viral meningitis Septic arthritis Syphilis Parvovirus B19 Infectious endocarditis Juvenile rheumatoid arthritis Reiter syndrome Brown recluse spider bite Fibromyalgia Chronic fatigue syndrome Treatment Remove tick: disinfect site then with blunt instrument, grasp tick proximal to skin and pull upward with gentle constant traction.  Mouthparts will release after about a minute. If residual mouthparts are left in skin, leave them alone to avoid infection (they will extrude from skin naturally over time).  Since ticks that have not attached or are moving on the skin cannot transmit Lyme, they can just be brushed off. NS IVF bolus, supportive care Cardiac monitoring, temporary pacemaker for heart block Beware Jarisch Herxheimer reaction: worsening of sx a few hours after treatment initiated Aspirin for cardiac involvement, NSAIDs for arthralgias/ arthritis Prophylaxis: Per the IDSA, give a single dose of 200 mg PO doxycycline to patients who meet all of the following criteria: Deer tick has been attached for 36 hours or more  (the rationale for time of attachment relates to the fact that the spirochetes live in the tick’s gut so they need a long time to multiply and travel to the salivary glands (event that’s triggered by a blood meal) and later overcome the salivary gland  (which only a few do) and finally reach the patient’ skin Prophylaxis can be provided within 72 hours of tick removal Local rate of B. Burgdorferi infection in ticks exceeds 20% (in the northeast USA, the prevalence of infected ticks is between 15-20%) Doxycycline can be used (children >8 years old, non-pregnant females) A 2001 study examined doxycycline vs placebo prophylaxis.  A single dose of 200 mg of oral doxycycline or placebo was given to persons presenting within 72 hours of removal of an I scapularis tick. One of 235 persons in the doxycycline group developed erythema migrans (EM) versus 8 of 247 in the placebo group, for treatment efficacy of 87% (95% CI, 25%–98%; P<0.04) (9). Reasonable alternative strategy: monitor for EM or other signs of infection then initiate treatment if they develop Lyme disease (excellent outcomes in patients treated during early EM stage of disease) Antibiotics: Antibiotics can speed resolution of arthritis and cardiac conduction delays, but not necessarily facial palsy Doxycycline has the best bioavailability and CNS penetration Always check with your ID colleagues to determine appropriate duration of treatment in more serious cases of Lyme disease Stage 1: Amoxicillin (500 mg PO TID) or cefuroxime (500 mg PO BID) or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 21 days; azithromycin (500 mg PO qday x 14-21 days) IV therapy in pregnant patients Stage 2: PO antibiotics for isolated Bell palsy and mild involvement Amoxicillin with probenecid (500 mg PO TID) x 30 days or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 10-21 days IV ceftriaxone (2 g IV qday) x 14-21 days, or penicillin G (20-24 million units IV q4-6h x 14-28 days) for meningitis, carditis, severe arthritis Stage 3: Penicillin G (20-24 million units IV q4-6h) x 14-21 days or ceftriaxone (2 g IV qday x 14-28 days) Dispotition Admit unstable or sick patients, those with meningoencephalitis, & carditis (telemetry/ ICU admission) DC patients treated with PO therapy Future prevention strategies: wear long pants & shirts, light-colored clothing (easier to spot crawling ticks), tuck pants into socks, DEET spray, clothing impregnated with permethrin References Baker C et al, Lyme Disease Review Panel of the Infectious Diseases Society of America (IDSA).  Final report of the lyme disease review panel of the infectious diseases society of America (IDSA). 2006.  https://www.idsociety.org/globalassets/idsa/topics-of-interest/lyme/idsalymediseasefinalreport.pdf (22 July 2019, date last accessed) Centers for Disease Control and Prevention.  CDC — Lyme. 2019. https://www.cdc.gov/lyme/index.html (22 July 2019, date last accessed) Hilton E, DeVoti J,, Benach JL, Halluska ML, White DJ, Paxton H, Dumler JS.  Seroprevalence and seroconversion for tick-borne diseases in a high-risk population in the northeast United States.  Am J Med. 1999 Apr;106(4):404-9. Hu LT.  Lyme Disease.  Ann Intern Med.  2016;164:ITC65-ITC80.  Doi: 10.7326/AITC201605030 Lee, M.  Lyme Disease.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  2015; 664-665. Nadelman RB, Nowakowski J, Fish D et al., Tick Bite Study Group.  Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite.  N Engl J Med.  2001;345:79-84. Sanders, L.  (2009). Every patient tells a story: Medical mysteries and the art of diagnosis. A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More
9 minutes | Jul 15, 2019
Episode 167.0 – Malaria
An in depth review of this notorious parasite. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Malaria.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Background In 2017, there were 219 million cases and 435,000 people deaths from malaria Five species: Falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. Falciparum, Vivax and Knowlesi can be fatal History of recent travel to Africa (69% of cases in US), particularly to west-Africa should raise suspicion for malaria Clinical Manifestations Average incubation period for Falciparum is 12 days 95% will develop symptoms within 1 month Clinical findings with high likelihood ratios include periodic fevers, jaundice, splenomegaly, pallor. Can also have vomiting, headache, chills, abdominal pain, cough, and diarrhea Severe malaria has a mortality of 5% to 30%, even with therapy Diagnostic criteria for severe malaria: Ashley 2018 Most common manifestations of severe malaria affect the brain, lungs, and kidneys Patients with cerebral malaria can present encephalopathic or comatose, some severe enough to exhibit extensor posturing, or seizures Can have acute lung injury with a quarter of these patients progressing to ARDS Can have AKI from ATN and resultant acidosis Labs may be unremarkable but watch for anemia and thrombocytopenia Hgb <5 has an OR = 4.9 for death Severe thrombocytopenia has an OR = 2.8 Anemia + Thrombocytopenia has an OR = 13.8 (Lampah 2015, PMID 25170106) Watch for hypoglycemia Be mindful of co-infection with salmonella and HIV Obtain BCx, cover with ceftriaxone Diagnosis Blood smear Thick smear to increase sensitivity for detecting parasites Thin smear for quantifying parasitemia and species The first smear is positive in over 90% of cases, but if suspicion is high, it has to be repeated BID for 2-3 days for proper exclusion of malaria (CDC 2019) Management For uncomplicated, non-severe cases, most patients with falciparum should be admitted, especially those with no prior exposure to malaria parasites Malarone is one of the first line options Check out other suggested regimens from the CDC Important to note that when they take this, ensure they take with milk or food containing fat to enhance absorption Severe Malaria Resuscitative efforts directed at affected organ Can deteriorate rapidly Initiate IV Artesunate if high level of suspicion Requires call to CDC: CDC Malaria Hotline: (770) 488-7788 or (855) 856-4713 (toll-free) Monday–Friday 9am–5pm EST – (770) 488-7100 after hours, weekends, and holidays Benzodiazepines for seizures Be judicious with fluids as this can precipitate pulmonary edema and cerebral edema a/w increased mortality in children at 48 hour (Maitland 2011, PMID: 21615299; Hanson 2013, PMID: 23324951) Take Home Points This is going to be a diagnosis that is mainly made through a thorough history, and pay particular attention to those with recent travel to West-Africa The incubation period for falciparum is 12 days, but there is a range of weeks and we should consider Malaria when consistent symptoms develop within 1 month of travel to an endemic area Typical signs and symptoms for uncomplicated malaria are periodic fevers, jaundice, pallor Be mindful of end organ involvement, such as cerebral edema, ATN, and pulmonary edema; these cases are considered to be severe and treated differently than uncomplicated  malaria Uncomplicated cases should get Malarone or Coartem Severe cases require IV Artesunate Be judicious with your fluid resuscitation as this can harm our patients References Centers for Disease Control and Prevention. CDC Parasites – Malaria. 2019 https://www.cdc.gov/parasites/malaria/index.html (7 July 2019, date last accessed) Ashley EA, Pyae Phyo A, Woodrow CJ. Malaria. Lancet. 2018;391(10130):1608-21. Hanson JP, Lam SW, Mohanty S, Alam S, Pattnaik R, Mahanta KC, et al. Fluid resuscitation of adults with severe falciparum malaria: effects on Acid-base status, renal function, and extravascular lung water. Crit Care Med. 2013;41(4):972-81. Lampah DA, Yeo TW, Malloy M, Kenangalem E, Douglas NM, Ronaldo D, et al. Severe malarial thrombocytopenia: a risk factor for mortality in Papua, Indonesia. J Infect Dis. 2015;211(4):623-34. Lokken KL, Stull-Lane AR, Poels K, Tsolis RM. Malaria Parasite-Mediated Alteration of Macrophage Function and Increased Iron Availability Predispose to Disseminated Nontyphoidal Salmonella Infection. Infect Immun. 2018;86(9). Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364(26):2483-95. Park SE, Pak GD, Aaby P, Adu-Sarkodie Y, Ali M, Aseffa A, et al. The Relationship Between Invasive Nontyphoidal Salmonella Disease, Other Bacterial Bloodstream Infections, and Malaria in Sub-Saharan Africa. Clin Infect Dis. 2016;62 Suppl 1:S23-31. Tintanelli, Judith E., et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eighth edition. New York: McGraw-Hill Education, 2016: p.1070-1077 World Health Organization. Guidelines for the treatment of malaria. Third edition April 2015. WHO. 2015 https://www.who.int/malaria/publications/atoz/9789241549127/en/ (7 July 2019, date last accessed) A special thanks to our editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine   Read More
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